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270 Cards in this Set
- Front
- Back
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Muscle Types |
-Skeletal: striated, voluntary -Smooth: not striated, involuntary -Cardiac: striated, involuntary Muscle cells are capable of shortening and converting the chemical energy of ATP into mechanical energy |
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Overall function of muscles |
Movement -Movement from place to place, movement of body parts and body contents in breathing, circulation, feeding and digestion, defecation, urination, and childbirth -Role in communication: speech, writing, nonverbal communications (ex. writing) Stability -Maintain posture by preventing unwanted movements -Antigravity muscles: resist pull of gravity and prevent us from falling or slumping over -Stabilizes joints Control of openings and passageways -Sphincters: internal muscular rings that control the movement of food, bile, blood, and other materials within the body Heat production by skeletal muscles -As much as 85% of out body heat Glycemic control -Regulation of blood glucose concentrations within its normal range |
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Characteristics of Muscle |
Excitability - (responsiveness) muscle responds to chemical signals, stretch and electrical changes across the plasma membrane Conductivity - local electrical change triggers a wave of excitation that travels along the muscle fiber leading to contraction Contractility - muscle shortens when stimulated Extensibility - muscle is capable of being stretched (most cells rupture when stretched to the degree of the muscle) Elasticity - muscle returns to its original resting length after being stretched |
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Muscle Compartments |
Deep fascia is found between adjacent muscles Superficial fascia (hypodermis) is mostly adipose tissue between skin and muscles -A group of functionally related muscles enclosed and separated from others by CT fascia -->Contains nerves and blood vessels that supply the muscle group (thoracic, abdominal walls, pelvic floor, limbs) -Intermuscular septa separate one compartment from another |
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Connective Tissue Elements |
Attachments between muscle and bone -endomysium, perimysium, epimysium, fascia, tendon (Collagen fibers of muscle CT are continuous with the collagen fibers in tendons and with the fibers of bone matrix) Collagen is somewhat extensible and elastic -stretches slightly under tension and recoils when released (protects muscle from injury/ returns muscle to its resting length) Elastic components -parallel components that are parallel to muscle cells (endomysium, perimysium, epimysium) -series components joined to ends of muscle (tendons or other connections to bone) -elastic recoil adds power output and efficiency of muscle |
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CT of Skeletal Muscle: Endomysium |
CT surrounding individual muscle cells, composed of reticular fibers, external lamina (basal lamina), and thin areolar tissue -allows room for capillaries and nerve fibers Innermost |
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CT of Skeletal Muscle: Perimysium |
Thicker CT that surround and defines fascicles (functional bundles of muscle fibers) Middle |
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CT of Skeletal Muscle: Epimysium |
Dense CT that surrounds the entire muscle (a collection of fascicles) -investing fascia to gross anatomy Outermost |
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Skeletal Muscle Overview |
Voluntary striated muscle attached to bones -Also attach to skin of the face, found in tongue and upper esophagus (visceral striated) Muscle fibers (myofibers) as long as 30cm Exhibits alternating light and dark transverse bands or striations -Reflects overlapping arrangement of internal contractile proteins Under conscious control (voluntary) |
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Muscle Fibers: Myofibers |
Contain multiple flattened nuclei inside cell membrane Development of myofibers: -fusion of multiple myoblasts during development -myoblasts fuse to form the skeletal muscle fiber (myofiber) -(myoblasts are the developmental precursor cells to skeletal muscle cells) -unfused satellite cells nearby can multiply to produce a small number of new myofibers (most muscle repair is by fibrosis rather than regeneration of functional muscle) -(Satellite cells between plasma membrane of the muscle fiber and its external lamina serve as stem cells for muscle regeneration - this process has limitations) |
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Muscle Fibers: Sarcolemma |
Sarcolemma has tunnel-like infolding or transverse (T) tubules that penetrate the cell -carry electric current to cell interior to trigger release of Ca2+ by the SR |
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Muscle Fibers: Sarcoplasm, SR & Triad |
Sarcoplasm is filed with myofibrils (bundles of myofilaments), glycogen (for stored energy) and myoglobin (for binding oxygen) Sarcoplasmic reticulum (SR) is smooth ER -forms a network around each myofibril -has dilated end-sacs (terminal cisternae) that traverse (travels across) the fiber and store calcium -Has gated channels in its membrane that open to release Ca2+ into the cytosol Triad = T tubule and 2 terminal cisternae |
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Myofilaments |
Each myofibril is a bundle of parallel protein microfilaments called myofilaments (Myofilament proteins are microfilaments inside of each myofibril)
There are 3 kinds of myofilaments: -Thick -Thin -Elastic |
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Thick Filaments |
Made of 200 to 500 myosin molecules -2 entwined polypeptides (golf clubs) Arranged in a bundle with heads directed outward in a spiral array around the bundled tails -Central area is bare zone with no heads |
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Myosin |
Composed of: -2 identical heavy chains : --> contain a globular head projecting from it at an angle, containing binding sites for actin & ATP --> tails aggregate forming thick filaments -2 pairs of light chains |
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Thin Filaments |
Composed of two intertwined strains of a protein called fibrous (F) actin -globular (G) (sub-unit of F actin) actin with an active site
Groove holds tropomyosin molecules (filaments bind in F-actin groove) -each blocking active sites of G actin
One small, calcium-binding troponin molecule on each tropomyosin molecule
Thin filament consists of 2 intertwined strands of (F) actin protein, which contains (G) actin subunits. Each G actin has an active site that can bind to the head of a myosin molecule. -Also contains tropomyosin, which blocks the active sites of G actin when the muscle fiber is relaxed (prevents binding of myosin). Each tropomyosin contains calcium-binding troponin proteins. |
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Thin Filament Components |
F-Actin: double-helical polymer of G-actin monomers Tropomyosin: filaments bind in F-actin groove Troponin: --TnT - binds to tropomyosin --TnC: binds Ca2+ --TnI: inhibits actin-myosin binding |
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Elastic Filaments |
-Made of springy proteins called titin ---Flank and anchor each thick filament to Z disc ---Helps to stabilize the thick filament, center it between the thin filaments, and prevents over- stretching of the sarcomere |
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Regulatory Proteins |
Tropomyosin and troponin -they start and stop shortening of muscle cell -contraction activated by release of calcium into sarcoplasm and its binding to troponin -troponin moves tropomyosin off the actin active sites |
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Contractile Proteins |
Myosin and actin |
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Striations |
Myosin and actin are not unique to muscle; these proteins occur in all cells -They function in cellular motility, mitosis and transport of intracellular materials -In skeletal and cardiac muscle they are especially abundant and organized in a precise array that accounts for striations |
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Organization of Filaments |
Dark A bands alternate with lighter I bands -anisotropic (A) and isotropic (I) stand for the way these regions affect polarized light A band = thick filament region -lighter, central H band (middle of A band) area contains no thin filaments I band = thin filament region -bisected (divided into 2 parts) by Z disc, anchoring elastic and thin filaments -from one Z disc to the next is a sarcomere |
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Relaxed and Contracted Sarcomeres |
Muscle cells shorten because their individual sarcomeres shorten -pulling Z discs closer together -pulls on sarcolemma (plasma membrane of muscle fiber) Notice neither thick nor thin filaments change length during shortening Their overlap changes as sarcomeres shorten |
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Dystrophin Protein |
-Dystrophin: cytoskeletal protein located beneath the sarcolemma in the vicinity of each I band and plays a role in linking F-actin in thin filament (via intermediate proteins) to laminin, an ECM protein, and ultimately to the endomysium
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Muscular Dystrophy |
Mutations in the dystrophin gene cause muscular dystrophies -Skeletal muscles degenerate and are replaced with adipose and fibrous tissue -Force of muscle contraction leads to torn cell membranes and necrosis Duchenne's muscular dystrophy (X-linked-mother carrier-disorder) causes progressive muscle weakness -Onset is between 3 & 5 yrs old and most cannot walk by 12 yrs of age, and at age 20 must use a respirator to breath -Children will appear to have large muscular calves, yet they continue to weaken : ---> focal fat replacement of muscle fibers in the biopsy ---> this fatty replacement, together with hypertrophic myofibers (thick fibers) and increased endomysial fibrosis (separates fibers ), is responsible for the pseudo-hypertrophy (fat and fibrous tissue infiltrate muscle tissue) seen in the calves of patients with Duchenne's -Diagnosed by muscle biopsy, blood enzymes, EMG, DNA testing -Biopsy myopathic features: atrophic & hypertrophic myofibers & increased endomysial fibrosis There are other milder forms of dystrophy (Becker muscular dystrophy progresses slower than Duchenne's) |
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Muscular Dystrophy Treatment |
Current treatment is designed to help prevent or reduce deformities in the joints and the spine and to allow people with muscular dystrophy to remain mobile as long as possible -Treatments may include various types of physical therapy, medications, assistive devices, and surgery -Medications: Anti-inflammatory corticosteroid prednisone may help improve muscle strength and delay the progression of Duchenne's |
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Compartment Syndrome |
Mounting pressure on the muscles, nerves, and blood vessels triggers a sequence of degenerative events: - Blood flow to compartment is obstructed by pressure - If ischemia (poor blood flow) persists for more than 2 to 4 hours, nerves begin to die - After 6 hours, muscles begin to die Nerves can regenerate after pressure is relieved, but muscle damage is permanent Myoglobin in urine indicates compartment syndrome Treatment: immobilization of limb and fasciotomy(procedure to cut fascia to relieve pressure/tension of muscle) |
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Severed Skeletal Muscle |
Skeletal muscle must be stimulated by a nerve or it will not contract If nerve connections are severed or poisoned, a muscle is paralyzed -Denervation atrophy: shrinkage of paralyzed muscle when connection is not restored |
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Somatic Motor Neurons |
Cell bodies of somatic motor neurons are in the brainstem and spinal cord Axons of somatic motor neurons are somatic motor fibers -terminal branches supply one muscle fiber |
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Motor Unit |
Each motor neuron and the all the muscle fiber it innervates is called a motor unit -All fibers of one motor unit belong to the same physiological type -They are dispersed throughout the muscle -When contracted together, it causes weak contraction over wide are -Provide the ability to sustain long-term contraction as motor units take turns resting (postural control) |
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Motor Unit: Small vs. Large |
Fine control -Small motor units contain as few as 20 muscle fibers per nerve fiber (ex. eye muscles, fingers) Strength and power -Large motor units contain 1000 muscle fibers (or more) per nerve fiber (ex. gastrocnemius (calf) muscle, gluteus maximus) |
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NMJ: Neurotransmitter |
Neuromuscular junction (synapse) in the functional connection between the nerve and muscle cell -Neurotransmitter (acetylcholine/ACh) is released from nerve fiber to stimulate muscle cell and initiate contraction |
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Neuromuscular junction components |
-Synaptic knobs are the swollen ends of nerve fibers -The muscle sarcolemma has junctional folds that increase surface area for ACh receptors (contains acetylcholinesterase that breaks down ACh and causes relaxation) -The synaptic cleft is the tiny gap between nerve and muscle cells -The basal lamina is a thin layer of collagen and glycoprotein surrounding the muscle fiber and the Schwann cell of the NMJ (separating them from the surrounding CT) and occupying the synaptic cleft -Mitochondria is abundant in the nerve terminal near the neurotransmitter filled vesicles -Axon terminals contain synaptic vesicles filled with ACh -Junctional folds in the muscle ACh receptors that bind the ACh that crosses the synaptic cleft |
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Pesticides |
Cholinesterase inhibitor -binds to acetylcholinesterase and prevents it from degrading ACh -causes spastic paralysis (state of continual contraction of the muscle) and possible suffocation |
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Tetanus |
A.k.a lockjaw -Spastic paralysis (state of continual contraction of the muscle) caused by toxin of Clostridium bacteria -->blocks glycine release in the spinal cord and causes overstimulation of the muscles (Glycine is an inhibitory neurotransmitter in the spinal cord) |
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Curare |
Flaccid paralysis (state in which muscles are limp and cannot contract) -Plant toxin (used for blowgun darts by South American natives) competes with ACh at nicotinic ACh receptors --> Causes respiratory arrest |
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Botulism |
Food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum - The toxin blocks the release of ACh and causes flaccid muscle paralysis (limp muscles) - It has been approved by FDA for treatment of muscle spasticity and for cosmetic treatment of "wrinkles" (Botox) |
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Resting Membrane Potential (RMP) |
The plasma membrane is polarized/charged - there are more (-) ions on the inside of the membrane than on the outside RMP is due to excess of Na+ and other cations outside of cell and excess anions (negative ions) inside of cell (proteins, nucleic acid, and phosphates) making the inside of the cell negative to the outside (unequal electrolyte distribution between ECF and ICF) -Results from: ions diffuse down their conc. gradient through membrane, plasma membrane is selectively permeable and allows some ions through, electrical attraction of cations and anions to each other -Membrane much less permeable to high conc. of Na+ found in ECF -Difference in charge across the membrane = resting membrane potential (-90 mV) --> Difference in electrical charge from one point to another is called an electrical potential, or voltage Na+/K+ pumps out 3 Na+ for every 2K+ it brings in (works continuous to compensate for Na+ and K+ leakage, and requires a lot of ATP) - ECF: 145 Na+ ---- 4 K+ - ICF: 12 Na+ ---- 150 K+ |
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Electrically Excitable Cells: Stimulation |
Stimulation opens ion gates in membrane - Ion gates open (Na+ rushes into cell and K+ rushes out of cell) --> The inside of the plasma membrane briefly becomes positive and this change is called depolarization --> It then becomes negative again (repolarization) --> Quick up-and-down voltage shift = action potential Action potential: dramatic change produced by voltage-regulated ion gates in the plasma membrane -Ions spread over cell surface in a similar manner as a nerve signal |
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Stimulated (active) cell process |
When stimulated: - Ion gates open in the plasma membrane - Na+ instantly diffuses down its concentration gradient into the cell - These cations override the negative charges in the ICF - Depolarization: inside of the plasma membrane becomes briefly positive - Immediately, Na+ gates close and K+ gates open - K+ rushes out of cell ---Repelled by the positive Na+ charge and partly because it is more concentrated in the ICF than in the ECF - Loss of positive K+ ions turns the membrane negative again (repolarization) - The quick change in voltage is called an action potential --- An action potential at one point on a plasma membrane causes another one to happen immediately in front of it - triggering a wave of action potentials that spread -----> Spread along a nerve fiber (nerve impulse/signal). These signals also travel the sarcolemma of a muscle fiber The 4 actions involved in this process: -Excitation (nerve action potentials lead to action potentials in muscle fiber) -Excitation-Contraction Coupling (action potentials on the sarcolemma activate myofilaments) -Contraction (shortening of muscle fiber) -Relaxation (return to resting length) |
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Excitation (steps 1-5) |
Steps 1-2: - Nerve signals open voltage-gated calcium channels in nerve synaptic knob - Calcium enters synaptic knob and stimulates exocytosis of ACh from synaptic vesicles - the vesicles are sent to and fuse with membrane - ACh is released into synaptic cleft and diffuses across Steps 3-4: - Two ACh molecules bind to each receptor protein on the sarcolemma of NMJ, opening NA+&K+ channels - Na+ enters, shifting RMP, which goes from -90mV to +75mV, then K+ exits and RMP returns to -90mV -- quick voltage shift is called an end-plate potential (EPP) Step 5: - Voltage change (EPP) in end-plate region opens nearby voltage-gated Na+&K+ channels producing an action potential that spreads over the muscle surface |
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Excitation-Contraction Coupling |
Refers to the events that link the action potential on the sarcolemma to action of the myofilaments for contraction |
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Excitation-Contraction Coupling (steps 6-9) |
Steps 6-7: -Action potential spreading over sarcolemma and enter T tubules. Voltage-gated channels in T tubules causes calcium gates to open in SR Steps 8-9: -Calcium released by SR binds to troponin -Troponin-tropomyosin complex changes shape and exposes active sites on actin for the myosin head |
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Contraction (steps 10-13) |
Myosin head must have an ATP bound Steps 10-11: -Myosin ATPAse in myosin head hydrolyzes an ATP molecule, activating the head "cocking" it in an extended position -It binds to actin active site forming a cross-bridge Steps 12-13: -Power stroke = myosin head releases ADP and phosphate as it flexes pulling the thin filament past the thick filament -With the binding of more ATP, the myosin head extends to attach to a new active side -->Half of the heads are bound to a thin filament at one time preventing slippage -->Thin and thick filaments do not become shorter, just slide past each other (sliding filament theory) |
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Relaxation (steps 14-18) |
Steps 14-15: - Nerve stimulation declines or stops & ACh release stops - Acetylcholinesterase (AChE) breaks down ACh (Choline is reabsorbed into synaptic knob for reuse) - Stimulation muscle by ACh stops Step 16: - Active transport is needed to pump calcium back into SR (calcium reabsorbed by SR). Calsequentin binds calcium in SR (protein stores calcium until stimulation reoccurs) - ATP is needed of muscle relaxation as well as muscle contraction Step 17-18: - Loss of calcium from sarcoplasm moves troponin-tropomyosin complex over active sites (stops the production or maintenance of tension) - Muscle fiber returns to its resting length due to recoil of series-elastic components and contraction of antagonistic muscles |
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Rigor Mortis |
Stiffening of the body beginning 3 to 4 hours after death -Deteriorating SR releases calcium -Calcium activates myosin-actin cross-bridging and muscle contracts, but cannot relax -Muscle relaxation requires ATP and ATP production is no longer produced after death -Fibers remain contracted until myofilaments decay |
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Myasthenia Gravis |
Characterized by progressive weakness that remits(refrains) with rest and is worsened by exercise -Autoimmune disease: antibodies attach NMJ by binding ACh receptors, on the post synaptic membrane, in clusters --> Antibodies bind to receptors, which block ACh from binding --> Receptor-antibody complex is removed by muscle fiber by endocytosis --> Functioning receptor sites are therefore reduced; and less and less sensitive to ACh (drooping eyelids (ptosis) and double vision often first signs, difficulty swallowing, weakness of the limbs, respiratory failure is possible while some people live normal lifespan) - More common in women between age 20 and 40 |
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Myasthenia Gravis Treatment |
-Cholinesterase inhibitors -Thymus removal dampens the immune response -Immunosuppressive agents such as prednisone and azathioprine (imuram) may be used to suppress the production of the antibodies that destroy ACh receptors -Plasmapheresis may be used to remove antibodies from blood plasma (not long-term option) |
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Length-Tension Relationship |
Amount of tension generated depends on length of muscle before it was stimulated -Overly contracted (weak contraction results): thick filaments too close to Z discs and can't slide -Too stretched (week contraction results): little overlap of thin and thick does not allow for very many cross bridges to form -Optimum resting length produces greatest force when muscle contracts (CNS maintains optimal length producing muscle tone or partial contraction) |
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Threshold |
Threshold is the voltage producing an action potential - A single brief stimulus at that voltage produces a quick cycle of contraction and relaxation called a twitch (lasting less than 1/10 second) |
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Phases of a Twitch Contraction |
-Stimulation -Latent period (2 msec delay): --> Only internal tension is generated --> No visible contraction occurs since only elastic components are being stretched -Contraction phase: --> External tension develops as muscle shortens -Relaxation Phase: --> Loss of tension and return to resting length as calcium returns to SR (A single twitch contraction is not strong enough to do any useful work) |
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Contraction Strength of Twitches |
-Threshold stimuli produces twitches -Twitches unchanged despite increased voltage -It is often stated that "Muscle fibers obeys an all-or-none law" contracting to its maximum or not at all --> This is not entirely true since twitches vary in strength - Depending upon, Ca2+ concentration, previous stretch of the muscle, temperature, pH and hydration -Increased stimulus frequency (closer stimuli) produce stronger twitches |
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Recruitment and Stimulus Intensity |
Stimulating the whole nerve with higher and higher voltage produces stronger contractions -Motor units are being recruited --->Called multiple motor unit summation --->Lift a glass of milk vs. a whole gallon of milk |
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Low Frequency Contraction |
Muscle stimulation at low frequency: -(up to 10 stimuli/sec) -Each stimulus produces an identical twitch response (Twitch) |
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Moderate Frequency Contraction |
Muscle stimulation at moderate frequency:
-(between 10-20 stimuli/sec)
-Each twitch has time to recover but develops more tension than the one before (treppe phenomenon)
--> Calcium is not completely put back into SR --> Heat of tissue increases myosin ATPase efficiency
(Treppe) |
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Higher Frequency Contraction/Stimulation |
(20-40 stimuli/sec) -Generates gradually more strength of contraction -Each stimuli arrives before last one recovers --> Temporal summation or wave summation Incomplete tetanus = sustained fluttering contraction |
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Maximum Frequency Contraction/Stimulation |
(40-50 stimuli/sec) -Muscle has no time to relax at all -Twitches fuse into smooth, prolonged contraction called complete tetanus -Rarely occurs in the body |
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Isometric Contraction |
Muscle contraction does not always mean shortening of a muscle -Develops tension without changing length -Contracts at the cellular level but tension is absorbed by the series-elastic components and is resisted by the weight of the load -Important in postural muscle function and antagonistic muscle joint stabilization (ex. no movement of the arm while holding a dumbbell, the muscle develops tension but does not shorten) |
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Concentric Isotonic Contraction |
(Isotonic contraction: change in length but no change in tension) Same tension while shortening -Begins when internal tension builds to the point that it overcomes the resistance -The muscle now shortens, moves the load, and maintains essentially the same tension from then on (ex. moving the arm up while holding a dumbbell, muscle shortens, tension remains constant) |
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Eccentric Isotonic Contraction |
Same tension while lengthening -The muscle lengthens, moves the load, and maintains essentially the same tension from then on. (ex. moving the arm down while holding a dumbbell, muscle lengthens, while maintaining tension - eccentric muscle contraction acts as a brake to keep from dropping the weight) |
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Pathways of ATP synthesis |
All muscle contraction depend on ATP Anaerobic fermentation (ATP production is limited): without oxygen, produces toxic lactic acid Aerobic respiration (more ATP produces): requires continuous oxygen supply, produces H20 and CO2 --- muscles use glucose during activity, but mostly fatty acids during rest |
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ATP Sources |
Short to intense exercise: -Aerobic respiration using oxygen from myoglobin -Phosphagen system -Glycogen-lactic acid system (anaerobic fermentation) -Aerobic respiration supported by cardiopulmonary function |
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Myoglobin in Aerobic Respiration (Immediate Energy Needs) |
Short, intense exercise (100m dash) -The respiratory and cardiovascular systems cannot deliver extra oxygen to muscles quickly enough for aerobic respiration -Myoglobin supplies a limited amount of oxygen for aerobic respiration |
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Phosphagen System (Immediate Energy Needs) |
Supplies most ATP for brief exercise -Myokinase transfers phosphate groups from one ADP to another forming ATP -Creatine kinase transfer phosphate groups from a phosphate storage molecule creatine phosphate to make ATP |
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Glycogen-Lactic Acid System (Anaerobic fermentation) (Short-term energy needs) |
Glycogen-lactic acid system takes over when phosphagen system is exhausted and until the cardiopulmonary function can catch up with the muscles' oxygen demand - Glycolysis produce enough ATP for 30-40 seconds of maximum activity (playing basketball or running around baseball diamonds) - Net gain of 2 ATP for each glucose molecule consumed and converted to lactic acid --> muscles obtain glucose from blood and stored glycogen |
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Aerobic Respiration (Long-Term Energy Needs) |
Needed for prolonged exercise -Produces 36 ATPs/glucose molecule After 40 seconds of exercise, respiratory and cardiovascular systems must deliver enough oxygen for aerobic respiration -Oxygen consumption rate increases for first 3-4 minutes and then levels off to a steady state -For exercise lasting more than 10 minutes, more than 90% of ATP is produced aerobically Limits are set by depletion of glycogen and blood glucose, loss of fluid and electrolytes |
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Fatigue |
Progressive weakness from prolonged use of muscles Causes: -ATP synthesis declines as glycogen is consumed ----> ATP shortage limits sodium-potassium pumps ability to maintain membrane potential and excitability -Lactic acid (lowers pH) inhibits enzyme function necessary for contraction -Accumulation of extracellular K+ hyperpolarizes the cell (lowers the membrane potential further, and makes fiber less excitable) ----> Each action potential releases K+ from the sarcoplasm to the ECF -Motor nerve fiber use up their acetylcholine (which leaves them less capable of stimulating muscle fibers) - this is termed junctional fatigue |
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Endurance |
Ability to maintain high-intensity exercise for more than 5 minutes -Determined by maximum oxygen uptake --->VO2 max is the point at which the rate of oxygen consumption reaches a plateau and does not increase further with added workload (it's proportional to body use, peaks at age 20, is larger in trained athletes and males) -Nutrient availability ---> Carbohydrate loading used by some athletes ===> packs glycogen into muscle cells ===> glycogen is hydrophilic - adds water at same time (2.7g water with each gram/glycogen) ===> (side effects include "heaviness" feeling |
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Resistance vs. Endurance Training |
Resistant: (aerobic) is the contraction of muscle against workload that resists movement -Prolonged exercise -Stimulates muscle growth -Muscle fibers synthesize more myofilaments and myofibrils grow thicker -Limits are set by depletion of glycogen and blood glycose, loss of electrolytes
Endurance: (aerobic) -Improves resistance -SO fibers produce more mitochondria and glycogen -Greater density of blood capillaries (conditioning) -Improves skeletal length, increases RBC count and oxygen transport capacity of blood -Enhances function of cardiovascular, respiratory, and nervous systems
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Oxygen Debt |
The difference between the resting rate of oxygen consumption and the elevated fate following an exercise ---- Known as excess post-exercise oxygen consumption (EPOC) ---- Heavy breathing for several minutes during and after strenuous exercise - occurs because body accrues an oxygen debt that must be repaid ---Replaces the body's oxygen reserves that were depleted ---Replenishes phosphagen system, oxidizes lactic acid and elevates metabolic rate |
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Types of Muscle Fibers |
-Slow twitch: Type I -Fast twitch: Type II(B) -Intermediate: Type IIA |
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Slow Twitch Fibers |
Slow oxidative, slow-twitch fibers, red, or Type I: - Have abundant mitochondria, myoglobin and capillaries - Appear deep red in color - Adapted for aerobic respiration and resistant to fatigue - In response to a single stimulus they exhibit a relatively long twitch -Low glycogen content, slow ATP hydrolysis - Examples: soleus (a calf muscle), and postural muscles of the back (100msec/twitch) are composed mainly of these high-endurance fibers (erector spinae, quadratus lumborum)
(Abundant in marathon runners - consistent/prolonged activity) |
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Fast Twitch Fibers |
Fast glycolytic, fast-twictch fibers, white, Type IIB - Rich in enzymes for phosphagen and glycogen-lactic acid systems (have fewer mitochondria, capillaries, and less myoglobin) - SR releases calcium quickly so contractions are quicker (7.5 msec/twitch) - Produce lactic acid and fatigue more readily -ATP synthesis through anaerobic respiration, poor fatigue resistance -Extraocular eye muscles, gastrocnemius and biceps brachii
(Abundant in sprinters and jumpers - "stop and go" activities) |
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Muscle Fiber Type |
Type IIA fibers are intermediate type that combine fast twitch responses with aerobic fatigue-resistant metabolism. They are relatively rare except in some endurance-trained athletes. All fibers of one motor unit belong to the same physiological type All muscles are composed of both type I (SO) and II (FG) but the proportions differ from one muscle to another Proportions of muscle type are genetically determined |
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Muscle Strength and Contraction |
-Muscle size (indicates strength - bigger muscles are stronger than smaller) and fascicle arrangement (cross-sectional area - pennate (interior thigh muscle) muscles are stronger than parallel muscles (eye muscle)) -Length-tension relationship: muscle at resting length can produce more force than one excessively shortened or stretched -Size of motor units (larger units produce stronger contraction) -Multiple motor unit summation: (when stronger muscle contraction is desired, the NS activates more motor units) recruitment of many motor units becomes more efficient with training, and can also occur under extreme stress -Temporal summation: (action potentials arriving at muscles) from nerve impulses -Fatigues muscle contract more weakly (than rested ones) |
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Cardiac Muscle Components |
Thick cells shaped, branched
Linked to each other at intercalated discs -Electrical gap junctions allow cells to stimulate their neighbors -Mechanical junctions keep the cells from pulling apart
SR is less developed but contains large T tubules that admit Ca2+ from ECF -T tubules are larger than in skeletal muscle and are located at a Z disc (Not at A-I junction as in skeletal muscle) -Diad (SR and T tubule) -Large mitochondria: span distance between T tubules -25% of cardiac muscle cell volume is occupied by mitochondria vs. about 2% for skeletal muscle -Striated
Damaged cells repaired by fibrosis, not mitosis (no satellite cells) |
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Cardiac Muscle |
Auto-rhythmic due to pacemaker cells (involuntary)
The heart also receives fibers from the autonomic nervous system that increase or decrease the rate and strength of contractility
Does not exhibit quick twitches like skeletal muscle, instead it maintains tension for about 200-250millisecs to allow the heart time to expel blood
Uses aerobic respiration almost exclusively -Large mitochondria make it resistant to fatigue -Very rich in mitochondria (filling 25% of the cell) as compared with skeletal muscle (2% of cell) -Very vulnerable to interruptions in oxygen supply |
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Myocardial Infarction |
- Death (necrosis) of cardiac muscle cells due to prolonged ischemia (lack of blood) - Usually repaired by fibrous CT so function is lost in this region of the heart - Serum cardiac specific troponin "cardiac enzymes" is measure to assess damage |
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Smooth Muscle Components |
Fusiform cells with one nucleus - 30 to 200 microns long and 5 to 10 microns wide - No striations, sarcomeres or discs - Thin filament attach to dense bodies scattered throughout sarcoplasm and on sarcolemma -Elongated, spindle shaped cells with a single centrally located nucleus - SR is scanty (small) and has no T tubules (Ca2+ for contraction comes from ECF) -Have no troponin - Calmodulin is the Ca2+ binding protein
If present, nerve supply is autonomic (releases either ACh or norepinephrine)
Capable of mitosis and hyperplasia - Pregnant uterus grows by adding more myocytes
Typically found in walls of hollow organs and blood vessels |
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Multiunit Smooth Muscle |
Largest arteries, iris, pulmonary air passages, arrector pili muscles of hair follicles, and iris of the eye Terminal nerve branches synapse on individual myocytes and form a motor unit Each motor unit contracts independent of the other motor units |
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Single-unit Smooth Muscle |
More widespread -Found in most blood vessels, and occurs in the digestive, respiratory, urinary, and reproductive tracts - it is thus often called visceral smooth muscle (In many hollow viscera there are 2 or more layers - typically as inner circular and outer longitudinal muscle layers) -Electrically coupled by gap junctions -Large number of cells contract as a unit |
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Stimulation of Smooth Muscle |
Involuntary and contracts without nerve stimulation - hormones, CO2, low pH, stretch, O2 deficiency - pacemaker cells in GI tract are auto-rhythmic (spontaneously depolarize) setting off waves of contraction throughout an entire layer of muscle ---> contract slower than cardiac muscle Autonomic nerve fibers have beadlike swellings called varicosities containing synaptic vesicles - Stimulates multiple myocytes at diffuse junctions - Have either norepinephrine or acetylcholine Nerve fibers have contrasting effects on smooth muscle in different locations - They relax the smooth muscle of arteries while contracting the smooth muscle in the bronchioles of the lungs |
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Smooth Muscle: Features of Contraction and Relaxation |
Calcium triggering contraction is from ECF instead of SR -Ca2+ channels triggered to open by voltage, hormones (ligand-gated channels), neurotransmitters or cell stretching ==> Ca2+ ions bind to calmodulin associated with thick filaments ==> Activates light-chain myokinase, which transfers a phosphate group from ATP to the head of the myosin, this then activates myosin ATPase and enables it to bind to actin ===> Power stroke occurs when ATP is hydrolyzed Thick filaments pull on the thin ones, the thin filaments pull on the dense bodies and membrane plaques. Intermediate filaments of cytoskeleton attach to dense bodies, then to the plasma membrane -Shortens the entire cell in a twisting fashion (like wringing out a wet towel) |
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Smooth Muscle: Contraction and Relaxation |
Contraction and relaxation are very slow in comparison (to skeletal muscle) because of slow myosin ATPase enzyme and slow pumps that remove Ca2+ Uses 10-300 times less ATP to maintain the same tension -Latch-bridge mechanism maintains tetanus (muscle tone) for a prolonged time without consuming ATP ==> Keeps arteries in state of partial contraction (vasomotor tone). A loss of this tone can cause a dangerous drop in blood pressure ==> Keeps intestines partially contracted |
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Smooth Muscle: Responses to Stretch |
Stretch opens mechanically-gated Ca2+ channels causing muscle response - Food entering the esophagus brings on peristalsis (muscle contractions that move food down digestive tract) Stress-relaxation response necessary for hollow organs that gradually fill (urinary bladder) - When stretched, tissue briefly contracts then relaxes Must contract forcefully when greatly stretched - Thick filaments have heads along their entire length - No orderly filament arrangement (no Z discs) Plasticity is ability to adjust tension to degree of stretch such as empty bladder and not become flabby |
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Histology of Skeletal Muscle |
Skeletal: striated, long parallel arrangement, multiple peripheral nuclei, cell shaped are lon -Location: associated with skeletal system -Cell shape: long-threadlike fibers -Striated -Multiple nuclei, adjacent to sarcolemma -CT: endomysium, perymysium, epimysium -SR: abundant -T tubules: narrow -No gap junctions -No auto-rhythmicity -Thin filament attachment: Z discs -Regulatory proteins: tropomyosin, troponin -Ca2+ source: SR -Ca2+ receptor: troponin of thin filament -Innervation and control: somatic motor fibers (voluntary) -Nervous stimulation required - Effect of nervous stimulation: Excitatory only -Mode of tissue repair: limited regeneration, mostly fibrous |
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Histology of Cardiac Muscle |
Cardiac: striated, branched cells, central nucleus, intercalated discs -Location: heart -Cell shape: short, slightly branched cells -Striated -Usually one nucleus, near middle of cell -CT: endomysium only -SR: present -T-tubules: wide -Gap junctions: present in intercalated discs -Autorhythmicity present -Thin filament attachment: Z discs -Regulatory proteins: tropomyosin, troponin -Ca2+ source: SR and ECF -Ca2+ receptor: troponin of thin filament -Innervation and control: autonomic fibers (involuntary) -Nervous stimulation NOT required -Effect on nervous stimulation: Excitatory or inhibitory -Mode of tissue repair: limited regeneration, mostly fibrous |
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History of Smooth Muscle |
Smooth: fusiform, central "cork screw" nucleus -Location: walls of viscera and blood vessels, iris of eye, pilo-erector of hair follicles -Cell shape: short fusiform cells -Not striated -One nucleus, near middle of cell -CT: endomysium only -SR: scanty -No T tubules -Gap junctions: present in single-unit smooth muscle -Autorhythmicity: present in single-unit smooth muscle -Thin filament attachment: dense bodies -Regulatory proteins: calmodulin, light-chain myokinase -Ca2+ source: mainly ECF -Ca2+ receptor: calmodulin of thick filament -Innervation and control: autonomic fibers (involuntary) -Nervous stimulation NOT required -Effect on nervous stimulation: excitatory or inhibitory -Mode of tissue repair: relatively good capacity for regeneration |
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Contracture |
Abnormal muscle shortening not caused by nervous stimulation. Can result from failure of the calcium pump to remove Ca2+ from the sarcoplasm or from contraction of scar tissue, as in burn patients |
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Cramps |
Painful muscle spasms triggered by heavy exercise, extreme cold, dehydration, electrolyte loss, low blood glucose, or lack of blood flow |
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Crush Syndrome |
A shock-like state following the massive crushing of muscles, associated with and potentially fatal fever, cardiac irregularities from K+ released from the muscle, and kidney failure resulting from blockage of the renal tubules with myoglobin released by the traumatized muscle. Myoflobinuria (myoglobin in urine) is a common sign |
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Delayed-onset muscle soreness |
Pain, stiffness, and tenderness felt from several hours to a day after strenuous exercise. Associated with micro-trauma to the muscles, with disrupted Z discs, myofibrils, and plasma membranes, and with elevated levels of myoglobin, creatine kinase, and lactate dehydrogenase in the blood |
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Disuse atrophy |
Reduction in the size of muscle fibers as a result of nerve damage or muscular inactivity, for example in limbs in a cast and in patients confined to a bed or wheelchair. Muscle strength can be lost at a rate of 3% per day of bed rest |
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Fibromyalgia |
Diffuse, chronic muscular pain and tenderness, often associated with sleep disturbances and fatigue; often misdiagnosed as chronic fatigue syndrome. Can be caused by various infectious diseases, physical or emotional trauma, or medications. Most common in women 30-50 years old |
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Myositis |
Muscle inflammation and weakness from infection or autoimmune disease |
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Overview of Nervous System |
Endrocrine and nervous system work together to maintain internal coordination of the body systems to maintain homeostasis
- Endocrine system coordinates activity via chemical messengers (hormones) delivered to the bloodstream - Nervous system coordinates activity via 3 basic steps: ==> Sense organs receive information ==> Brain and spinal cord determine responses ==> Brain and spinal cord issue commands to glands and muscles |
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Subdivisions of Nervous System |
Central nervous system (CNS) - Brain and spinal cord Peripheral nervous system (PNS) - Neves and ganglia |
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Central Nervous System (CNS) |
Brain and spinal cord enclosed in bony covering (cranium and vertebral column) |
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Peripheral Nervous System (PNS) |
Consists of the nervous system outside the brain and spinal cord. It is composed of nerves and ganglia - A nerve is a bundle of axons (nerve fibers) wrapped in CT - A ganglion is a swelling or bulbous region of a nerve where the cell bodies of neurons are concentrated |
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Functional Divisions of PNS: Sensory |
Sensory (afferent) (carry sensory signals from many receptors - sense organs & simple sensory nerve endings) to CNS) Divisions (receptors to CNS): - Visceral sensory: heart, lungs, stomach, bladder, etc. (mainly from thoracic and abdominal cavity) - Somatic sensory: skin, muscles, bones, joints |
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Functional Divisions of PNS: Motor |
Motor (efferent) (carry signals from CNS to glands and muscle cells that carry out body's responses) Divisions (CNS to effectors): - Visceral motor division - Autonomic NS (ANS)(carry signals to glands, cardiac muscle, and smooth muscle) - Effectors: cardiac, smooth muscle, glands ==> Sympathetic division (arouse the body for action) ==> Parasympathetic division (slow the body, increase digestion) - Somatic motor divisions (signal to skeletal muscles) - Effectors: skeletal muscle |
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Properties of Neurons |
The communicative role of the nervous system is carried out by nerve cells (neurons): Excitability (irritability) -Ability to respond to changes in the body and external environment called stimuli Conductivity -Produce traveling of electrical signals that are quickly conducted to other cells at distant or nearby locations Secretion -When electrical signal reaches end of nerve fiber, a chemical neurotransmitter is secreted that crosses the gap (synapse) and stimulates the next cell |
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Sensory (afferent) Neurons |
Detect changes in body and external environment (stimuli) and transmit this to brain or spinal cord - Carries signals from receptors in the skin, muscles, bones and joints (somatic sensory) - Carries signals from internal organs (visceral sensory) - Taste and hearing have special receptors that relay signals to sensory neurons - Some neurons carry signals of pain and smell that the neurons detect directly (Afferent neurons carry signals to the CNS) |
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Interneurons (association neurons) |
Lie between sensory and motor pathways in CNS - 90% of our neurons are interneurons - Process, store and retrieve information (determine how the body responds to stimuli) - performing an integrative function |
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Motor (efferent) Neuron |
Send signals out to muscles and gland cells (away from the CNS) -Somatic motor neurons carry signals to the skeletal muscles (voluntary and reflexes) -Visceral motor neurons (autonomic nervous system) carry signals to glands, cardiac muscle, and smooth muscle of organs and blood vessels (involuntary, visceral reflexes) ==> Autonomic nervous system has 2 primary divisions: sympathetic & parasympathetic Efferent neurons carry signals from the CNS to effectors (muscles or organs). Organs that carry out responses called effectors |
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Structure of a neuron: cell body |
Cell body of a neuron is the perikaryon or soma (control center of the neuron) - Single, central nucleus with large nucleolus - Cytoskeleton of microtubules and neurofibrils (bundles of actin filaments), which compartmentalize RER into Nissl bodies - Mitochondria, lysosomes, Golgi - Cytoplasmic inclusions: lipofuscin, glycogen granules, and melanin in some neurons |
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Lipofuscin |
Golden brown pigment, product of breakdown of worn out organelles (cannot be digested by lysosomes) -Accumulates with age in post mitotic cells such as neurons and cardiac myocytes |
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Structure of a Neuron: Dendrites |
Processes that branch from the soma - They are the primary site for receiving signals from other neurons - The more dendrites a neuron has, the more information it can receive and incorporate into its "decision making" |
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Structure of a Neuron: Axon |
Single axon (nerve fiber) arising from axon hillock for rapid conduction - The axon is cylindrical and relatively unbranched for most of its length - The axon hillock is on one side of the soma where the soma tapers and gives rise to the axon -Axons tend to have uniform diameters along their entire length -Axon cytoplasm is called axoplasm and its membrane axolemma -They do not taper like dendrites and their contours are smooth - Axons branch at obtuse angles and can have branches called collaterals, that come off at right angles - Often, when an axon reaches a target area, it branches. The terminal arborations (branches) of axons are called telodendria - Each branch ends in a synaptic knob (terminal button), a little swelling that forms a junction (synapse) with the next cell - An axon is specialized for rapid conduction of nerve signals to points remote from the soma |
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Axons Ultrastructure |
Both microtubules and neurofilaments are found in axons -Microtubules are important as tracks for fast anterograde and retrograde axonal transport -Neurofilaments predominate (are more abundant that microtubules) and are believed important in maintaining axonal diameter |
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Additional Neuronal Cell Body Features |
The neuron is a highly active cell as evidenced by a prominent nucleolus within a euchromatic nucleus -Neuronal cytoplasm is typically basophilic (takes up basic dyes-appears blue/purple) -The basophilia can be seen to occur in clumps called Nissl bodies ==> Nissl bodies are made up of RER and polysomes ==> Reflect the high level of synthesis of membrane and secreted products (neurotransmitters) |
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Neurofibrillary tangles |
Prominent feature of degeneration neurons in Alzheimer's disease, amyotrophic lateral sclerosis (ALS), and Down syndrome (buildup of protein in neurons) |
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Variation in Neural Structure |
Multipolar neuron: most common, many dendrites per one axon (The more dendrites a neuron has, the more information it can receive and incorporate into its "decision making process" Bipolar neuron: one dendrite per one axon (olfactory, retina, ear) Unipolar (pseudounipolar) neuron: sensory from skin and organs to spinal cord Anaxonic neuron: many dendrites-no axon, help in visual processes in retina |
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Axonal Transport |
All proteins needed by a neuron must be made in the soma - It is the location of nucleus, ribosomes and RER Many proteins made in soma must be transported to axon and axon terminal - In order to repair the axolemma, for gated ion channel proteins, as enzymes, or neurotransmitters -Slow and fast axonal transport ----> Fast (rate of 20-40mm/day): anterograde or retrograde) |
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Slow Axonal Transport |
-Occurs at a rate of 0.5-10mm/day -Conveys structural elements: tubulin, neurofilament proteins, actin -Only anterograde (away from soma, down the axon) |
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Fast Axonal Transport (Anterograde) |
-For organelles, enzymes, vesicles and small molecules -Anterograde component conveys membraneous organelles and membrane-bound proteins away from cell body toward axon terminals ==> Mitochondria ==> Synaptic vesicles ==> SER -Microtubule dependent -Uses kinesin as a motor protein (away from soma, down the axon) |
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Fast Axonal Transport (Retrograde) |
- Retrograde component conveys worn out organelles and endocytosed materials (recycled material) such as growth factors, toxins and viruses -Microtubule dependent -Uses dynein as a motor protein (Pathogens take this route back to the soma) (toward soma, up the axon) |
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Microtubule disruptors |
Substances that disrupt microtubules or that prevent their assembly will prevent or inhibit fast axonal transport -Colchicine and vinblastine can cause axonal polyneuropathy because they disrupt microtubule assembly |
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Retrograde Transport of Viruses |
A number of viruses exhibit mimicry (they express on their surfaces epitopes (antigenic determinate, can stimulate an immuse response) that allow them to bind to neuronal receptors)
-Rabies virus binds to the acetylcholine receptor of motor neurons innervating infected muscle cells - it is retrogradely (toward soma) transported to cell body where the virus can replicate (nucleus)
-Polio, herpes, and rabies viruses are taken up and follow retrograde transport in axons ==> Sensory neurons, in the case of herpes virus, are the target. The virus remains dormant in sensory ganglia (cell body of the sensory neuron) |
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Types of Neuroglial Cells |
There are 6 types of neuroglia, each with a unique function. 4 types occur only in the CNS: -Oligodendrocytes -Ependymal cells -Microglia -Astrocytes 2 types occur only in the PNS: -Schwann cells -Satellite cells |
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Neuroglial Cells: Oligodendrocytes |
Form myelin sheaths in CNS - Each wraps around many nerve fibers |
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Neuroglial Cells: Ependymal Cells |
Line cavities filled with cerebrospinal fluid (CSF) - Choroid plexus cells produces CSF |
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Neuroglial Cells: Microglia (macrophages) |
Formed from monocytes - Phagocytose dead tissue, microorganisms, foreign matter - Concentrate in areas of infection, trauma, stroke, and neoplastic cells |
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Neuroglial Cells: Astrocytes |
Most abundant glial cells - form framework of CNS –Contribute to BBB and regulate composition of brain tissue fluid ==>Have extensions called pervascular feet, which contact the blood capillaries and stimulate them to form a tight seal (tight junctions) called the blood-brain barrier. –Convert glucose to lactate to feed neurons –Secrete nerve growth factor promoting synapse formation –Absorb neurotransmitters and potassium ions released by neurons (regulate fluid composition around synapse) –Sclerosis: damaged neurons replace by hardened mass of astrocytes |
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Neuroglial Cells: Schwann Cells |
Myelinate axons in the PNS and assist in regeneration of damaged nerve fibers |
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Neuroglial Cells: Satellite Cells |
Found around peripheral nerve ganglia and have uncertain function |
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Glial Tumors Overview |
Mature neurons are post mitotic and seldom form tumors - New research shows neurons regenerate in the certain regions such as the hippocampus |
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Astrocytic tumors (astrocytomas) |
Tumors involving cells derived from astrocytes are the most common type of primary brain tumor. They comprise 80-90% of all glial tumors in adults. – Gliomas usually grow rapidly and are highly malignant. – Frequently disseminate via the CSF to other regions of the CNS, but seldom metastasize to the rest of the body – Because of BBB, brain tumors usually do not yield to chemotherapy and must be treated with radiation or surgery. – Mean survival 8-10 months |
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Myelin |
Insulating layer around a nerve fiber (axon) -Oligodendrocytes in CNS and Schwann cells in PNS -formed by wrappings of plasma membrane: 20% protein and 80% lipid (looks white) - Lipid includes: phospholipids, glycolipids, cholesterol -Myelination proceeds rapidly in infancy and is complete by adolescence -Gaps between myelin segments are termed nodes of Ranvier -Initial segment (area before 1st schwann cell) and axon hillock form trigger zone where signals begin |
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Myelin in PNS |
- Schwann cell spirals repeatedly around a single nerve fiber (axon), laying down many layers of compact membrane (myelin sheath) with almost no cytoplasm between the membranes; it spirals outward as it wraps the nerve fiber, ending with a thick outermost coil(neurilemma), where it contains its nucleus and most of its cytoplasm. External the neurilemma is the basal lamina, then a thin sleeve of fibrous CT(endoneurium). -Unmyelinated nerve fibers are enveloped in Schwann cells (it holds small nerve fibers in grooved on their surface withonly one membrane wrapping) |
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Myelin in CNS |
- Each oligodendrocyte reaches out to myelinate several nerve fibers in its immediate vicinity. Since it’s anchored to multiple nerve fibers, it cannot migrate around any one of them like a Schwann cell does. It must push newer layers of myelin under the older ones, so myelination spirals inward toward the nerve fiber. Nerve fibers of the CNS have no neurilemma or endoneurium. |
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Multiple Sclerosis |
Chronic demyelination disease of the CNS -Multiple, focal plaques of demylenization -Optic nerve, which is myelinated by oligodendroglia, if often affected
Immune system eats away protective covering (myelin) of nerves
May be autoimmune -Antibodies to CNS myelin (myelin basic protein)
Characterized by remission and relapse (improvement and worsening)
CNS plaques (scars) formed by astrocytes in the white matter
Nerve conduction is disrupted
Ages 20-40
Symptoms in declining order of frequency: –Unilateral visual impairment. –Diplopia (double vision). –Paresthesias(pins and needles) –Ataxia (unsteadiness) –Vertigo (dizziness) –Fatigue –Paresis (muscle weakness) –Dysarthria (speech problems) –Mental disturbances
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Tay Sachs Disease |
Hereditary disorder of infants of Eastern European Jewish ancestry - Abnormal accumulation of glycolipid called GM2 in the myelin sheath (disrupts conduction of nerve signals) --- Normally decomposed by lysosomal enzyme --- Enzyme missing in individual homozygous for Tay-Sachs allele --- Blindness, loss of coordination, and dementia
-Fatal before age of 4
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Speed of Nerve Signal |
The speed at which a nerve signal travels along a nerve fiber depends on: Diameter of fiber and presence of myelin -- Large fibers have more surface area for signals
Speeds: -- Small, unmyelinated fibers: 0.5-2m/sec -- Small, myelinated fibers: 3-15m/sec -- Large, myelinated fibers: up to 120m/sec
Functions: -- Slow signals supply the stomach and dilate pupil -- Fast signals supply skeletal muscles and transport sensory signals for vision and balance |
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Regeneration of Peripheral Nerves |
-Occurs if soma and nerilemma tube is intact -The stranded end of the axon and myelin sheath degenerate (cell soma swells, ER breaks up and some cells die) -Axon stump puts out several sprouts -Regeneration tube (Schwann cells, basal lamina, and the neurilemma) guides axonal sprout back to its original destination ===>Schwann cells produce nerve growth factors and cell-adhesion molecules -Soma returns to its normal appearance |
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Action Potential of Neurons |
Action potential: rapid up-and-down shift in the membrane voltage
- Only occurs where there is a high enough density of voltage-regulated gates - Soma (50 to 75 gates per nm^2) - Trigger zone (350 to 500 gates per nm ^2); where action potential is generated : if excitatory local potential spreads all the way to the trigger zone and is still strong enough when it arrives, it can open these gates and generate an action potential
-Na+ ions arrive at the axon hillock, and depolarize the membrane -Threshold: critical voltage to which local potentials must rise to open the voltage-regulated gates (-55mV) -When threshold is reached, neuron "fires" and produces an action potential -More and more Na+ channels open in the trigger zone in a positive feedback cycle creating a rapid rise in membrane voltage (spike) -Only a thin layer of the cytoplasm next to the cell membrane is affected (very few ions involved)
-Nondecremental: does NOT get weaker with distance -Irreversible: once started, it goes to completion and cannot stop |
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Local Potential |
-Produced by gated channels on dendrites and soma -May be positive (depolarization) or negative (hyperpolarization) voltage change -Graded - proportional to stimulus strength -Reversible: returns to RMP if stimulation stops before threshold is reached -Local: has effects for only a short distance from point of origin -Decremental: signal grows weaker with distance |
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Salutatory Conduction |
Propagation of a nerve signal that seems to jump from node to node. -Action potentials occurs at the nodes (influx of Na+ gates), and the nerve signal appears to jump from node to node |
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Refractory Period |
Refractory period: the period of resistance to stimulation -- During an action potential and for a few milliseconds after, it's difficult or impossible to stimulate that region of a neuron to fire again
-- Refers only to a small patch of the neuron's membrane at one time -- Other parts of the neuron can be stimulated while the small part is the refractory period
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Refractory Period Phases |
Two phases:
Absolute refractory period: no stimulus of any strength will trigger an action potential, as long as Na+ gates are open (from action potential to RMP)(impossible)
Relative refractory period: only especially strong stimulus will trigger an action potential - K+ gates are still open and any effect of incoming Na+ is opposed by the out K+ (Difficult) |
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Overview of Spinal Cord |
Carries information between brain and body -Extends through vertebral canal from foramen magnum (opening at the base of the skull) to the level of the 2nd lumbar vertebra (L2) -Each pair of spinal nerves receives sensory information and sends motor signals to muscles and glands -Spinal cord is a component of the CNS |
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Functions of the Spinal Cord |
Conduction - Bundles of fibers passing info up and down spinal cord allowing sensory info to reach brain and motor commands to reach effectors
Locomotion - Repetitive, coordinated actions of several muscle groups ==> Motor neurons in the brain initiate walking and determine speed, distance, direction ==> Central pattern generators are pool of neurons in the spinal cord providing alternating movements of flexors and extensors (walking)
Reflexes - Involuntary, stereotyped responses to stimuli (remove hand from hot stove) - Reflexes involve the brain, spinal cord and peripheral nerves |
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Anatomy of the Spinal Cord |
Cylinder of nerve tissue within the vertebral canal (thick as a finger): adult the spinal cord only extends to L1-L2 (lumbar vertebral levels)
31 pairs of spinal nerves arise from the spinal cord - each cord segment gives rise to a pair of spinal nerves (They are mixed nerves containing both motor and sensory fibers, which exit at the intervertebral fomaren and then branch) - Distal branches of nerves: ==> Dorsal ramus supplies dorsal body muscle and skin ==> Ventral ramus to ventral skin and muscles and limbs ==> Meningeal branch to meninges, vertebrae and ligaments
There are cervical and lumbar enlargements
Medullary cone (conus medullaris) is the tapered tip of cord
Cauda equinae is L2 to S5 nerve roots (resembles a horse's tail) |
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Meninges of the Spinal Cord |
The spinal cord and brain are enclosed in three fibrous CT membranes called meninges - They separate soft tissue of CNS from bones of vertebrae and skull - From superficial to deep: dura mater, arachnoid mater, pia mater |
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Meninges: Dura Mater |
(tough mother) -Tough collagenous membrane surrounded by epidural space filled with fat and blood vessels ---> Epidural anesthesia utilized during childbirth |
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Meninges: Arachnoid Mater |
(spider web resembling) - Layer of simple squamous epithelium lining the dura mater and loose mesh of fibers filled with CSF (creates subarachnoid space) |
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Meninges: Pia Mater |
Delicate membrane adherent to spinal cord |
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Spina Bifida |
-Congenital (present at birth) neural tube (embryo's precursor to the CNS) defect in 1 baby out of 1000 - Failure of vertebral arch to close covering spinal cord - Folic acid as part of a healthy diet for all women of childbearing age reduces risk - deficiency increases risk - Certain anti-seizure medications can cause neural tube defects like spina bifida, if high doses of folic acid are not given along with the drugs during early pregnancy |
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Cross-Sectional Anatomy of Spinal Cord |
Central area of gray matter (shaped like a butterfly and surrounded by white matter in 3 columns) Gray matter has neuron cell bodies with little myelin - Pair of dorsal (posterior) horns: dorsal root of spinal nerve is all sensory fibers (input to spinal cord) - Pair of ventral (anterior) horns: ventral root of spinal nerve is all motor fibers (output of spinal cord) ---> Connected by gray commisure White matter has myelinated axons - White columns are bundles of myelinated axons that carry signals up and down to and from brainstem (3 pairs of columns or funiculi: dorsal, lateral, and anterior) - Each column is filled with named tracts or fasciculi (fibers with a similar origin, destination and function) |
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Spinal Tract Terms |
-Ascending and descending tracts head up and down while decussation means that the fibers cross sides -Contralateral means that the origin and destination are on opposite sides -Ipsilateral means same side |
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Ascending Tracts/Pathways |
Ascending tracts carry sensory signals up the spinal cord -Sensory signals typically travel across three neurons from their origin in the receptors to their destination in the sensory areas of the brain - 1st order neuron: detects stimulus - 2nd order neuron receives stimulus from 1st order neuron and sends it up to the thalamus at upper end of brain stem ("the getaway" - 3rd order neuron carries stimulus from the 2nd order neuron in the thalamus to the region of the sensory cortex of the cerebrum Ascending tracts: Gracile fasciculus, Cuneate fasciculus, spinothalamic tract, spinoreticular tract, posterior (dorsal) and anterior (ventral) spinocerebellar tracts |
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Somatosensory Systems |
Postcentral gyrus is primary sensory cortex: organized somatotopically (sensory humunculus - "little man") Two major sensory pathways: -Dorsal columns (lemniscal system) : discriminative touch, proprioception, and vibratory sense --->Crosses (decussates) in the medulla Anterolateral (spinothalamic) system: crude touch, pain and temperature --->Crosses (decussates) in the spinal cord |
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Dorsal Column Ascending Pathway |
-Deep touch, vibration, and proprioception are carried in the dorsal columns (Fasciculus gracilis and cuneatus carry signals from leg and arm)
-1st order neuron travels up the ipsilateral spinal cord terminating in the medulla oblongata -Decussation of 2nd order neuron in medulla (form the medial lemniscus) a tract that head up to the thalamus) -3rd order neuron in thalamus carries signal to cerebral cortex |
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Spinothalamic Pathway (ascending) |
Pain, pressure, temperature, light touch, tickle and itch are carried in the spinothalamic pathway -1st order neuron ends near its point of entry (the dorsal horn) -Decussation of the 2nd order neuron occurs in spinal cord -3rd order neurons arise in thalamus and continue to cerebral cortex (contralateral) |
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Sensory loss and spinal cord injury |
Injury to the spinal cord will cause loss of pain and temperature sense on the contralateral side below the lesion (spinothalamic pathway) --Such injury will cause ipsilateral loss of fine (discriminative) touch, proprioception and vibration below the lesion (dorsal column ascending pathway) |
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Spinocerebellar Pathway (ascending) |
-Proprioceptive signals from limbs and trunk travel up to the cerebellum -Tracts and side of cerebellum responsible for body is ipsilateral |
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Descending Tracts |
Carry motor signals down the brainstem and spinal cord Involve two neurons: - Upper motor neuron originates in cerebral cortex or brainstem and terminates on a lower motor neuron - Lower motor neuron in brainstem or spinal cord: axon of lower motor neuron leads the rest of the way to the muscle or other target organ -Lower motor neurons reside in anterior horn of spinal cord ----> Their axons innervate skeletal muscle, form the motor portions of peripheral nerves, are called " the final common pathway" since they receive input from higher brain areas such as cerebral cortex) -Upper motor neurons are higher centers such as the motor cortex ----> Their axons excite or inhibit lower motor neurons |
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Corticospinal tract (descending - lateral) |
Clinically most important descending tract -Arises from upper motor neurons in the motor cortex (motor cortex is somatotopically organized) -Axons descend and cross in the pyramidal decussation in the caudal medulla (pyramids) -Innervates lower motor neurons which innervate limb muscles -Carry motor signal from the cerebral cortex for precise, coordinated limb movements) Two neuron pathway: - Upper motor neuron in cerebral cortex descends to cord and synapses in the ventral horn with the lower motor neuron - Lower motor neuron cell body is in the ventral horn of the spinal cord |
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Upper Motor Neuron Injury |
Injury of corticospinal system (pyramidal tract) anywhere above the pyramidal decussation (medulla) causes contralateral paralysis of the limbs Injury below the pyramidal decussation will cause ipsilateral paralysis below the lesion |
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Spinal Cord Trauma |
10-12,000 people/year are paralyzed, 55% occur in traffic accidents -Spinal cord injury poses risk of respiratory failure if segments innervating the diaphragm or above are damaged -Early symptoms are called spinal shock (few days to weeks), flaccid paralysis, loss of sensation below lesion and absence of reflexes -Later, hypereflexia occurs (both somatic and autonomic) -Tissue damage at time of injury is followed by post-traumatic infarction -Complete transection of the spinal cord causes immediate loss of motor control at and below the level of injury -Treatment: stabilize spine to prevent further injury; methylprednisolone (steroid drug) given early after injury dramatically improves recovery by reducing injury to cell membranes, inhibiting inflammation, and apoptosis (prevents the spread of damage to several spinal cord adjacent segments); surgery to stabilize fractures; physical therapy for rehab and adaptive equipment |
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Polio & ALS |
Diseases causing destruction of motor neurons and skeletal muscle atrophy Poliomyelitis caused by poliovirus spread by fecal contaminated water -- Destroys motor neurons in the brainstem and ventral horn of the spinal cord -- Muscle pain, weakness progresses to paralysis, and potentially respiratory arrest Amyotrophic Lateral Sclerosis (Lou Gehrig disease) -- Degeneration of motor neurons and atrophy of muscles -- Sclerosis of lateral regions of spinal cord: astrocyte failure to reabsorb glutamate neurotransmitter - becomes neurotoxic -- Paralysis and muscle atrophy |
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Guillain-Barre |
Guillain-Barre syndrome (a.k.a. acute inflammatory demyelinating polyadiculoneuropathy) : one of the most common, life-threatening diseases of the PNS, it is often triggered by a viral infection Large segments of the myelin sheath are damaged -Large accumulations of lymphycytes, macrophages and plasma cells around nerve fibers within nerve fasicles T cell-mediated immune response directed against myelin causing its destruction and slowing or blocking nerve conduction Symptoms are of ascending muscle paralysis, loss of muscle coordination, and loss of cutaneous sensation, sometimes death from respiratory paralysis |
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Anatomy of a Spinal Nerve |
A nerve is a bundle of nerve fibers (axons) -Epinerium corvers nerves, perineurium surrounds a fascicle and endoneurium separates individual nerve fibers -Blood vessels penetrate only to the perineurium (epineurium + perineurium) |
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Local Anesthetics & Nerves |
Local anesthetics, such as lidocaine, act by blocking the cytoplasmic side of the voltage-gated Na+ channel. The hydrophobicity of the anesthetic determines how efficiently if diffuses across lipid membranes and how it binds to the Na+ channel, and therefore its potency Local anesthetics are injected or applied outside the peripheral nerve epineurium and therefore must cross the epineurium to reach the perineurium, which is the most difficult layer to penetrate because of tight junctions between cells -- Anesthetics then pass through the endoneurium, which invests the myelinated and unmyelinated fibers, Schwann cell and capillaries -- Only anesthetics that have passed through these 3 sheaths can reach the neuronal membrane where the voltage-gated Na+ channels that affect nerve conduction reside |
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Cutaneous Innervation and Dermatodes |
Each spinal nerve receive sensory input from a specific area of skin called dermatode -Overlap at edges: a total loss of sensation requires anesthesia of 3 successive spinal nerves |
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Shingles |
Skin eruptions along the path of sensory nerves - Varicella-zoster virus (chicken pox) remains from like in dorsal root ganglia -Occurs after age 50 if immune system is compromised ==> Travels back down the sensory nerves by fast axonal transport causing skin disocoloration and fluid dilled vesicle along the cutaneous region of the nerve ==> Antiviral drugs (acyclovir) can shorten the course of an episode of shingles if taken with the first 2-3 days of outbreak ==> Post herpetic neuralgia (pain due to varicella virus that causes outbreak of skin) can cause intense pain along the course of the nerve for months of even years and it's difficult to treat |
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Radiculopathies |
Sensory or motor dysfunction caused by injury to a nerve root - Injuries to posterior (dorsal) roots cause sensory disturbances - Injuries to anterior (ventral) roots cause motor disturbances Commonly, radiculopathies are due to vertebral disc herniation Often, burning pain or tingling radiates in affected dermatode Motor deficits may result in muscle paresis (weakness), atrophy and fasciculation - Muscles are not normally paralyzed if only one root is affected (For example, if the C6 anterior root is injured, the biceps is weak, not paralyzed) |
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Neuropathies |
Sensory or motor dysfunction caused by pathology affecting a nerve Neuropathies can result from metabolic disorders such as diabetes mellitues - Diabetic neuropathy: glove and stocking (numbness or tingling feeling sensation in a stocking and glove distribution - entire foot is affected) Can manifest as burning pain or tingling radiates in affected nerve distribution Sensory deficits involve portions of adjacent dermatodes Motor neuropathies cause muscle paralysis, atrophy, and fasciculation |
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Muscle Reflexes |
Somatic reflexes are quick, involuntary, stereotyped reactions of glands or muscle to sensory stimulation - Automatic responses to sensory input that occurs without our intent or often even our awareness |
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Somatic Reflex Arc Functions |
-Stimulation of somatic receptors -Afferent fibers carry signal to dorsal horn of spinal cord -One or more interneurons integrate the information -Efferent fibers carry impulses to skeletal muscles -Skeletal muscles respond |
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Muscle Spindle |
Sense organ (proprioception) that monitors length of muscle and how fast muscles change in length Composed of intrafusal muscle fibers, afferent fibers, and gamma motor-neurons |
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Stretch (Myotatic) Reflex |
When a muscle is stretched, it contracts and maintains increased tonus (stretch reflex) - Helps maintain equilibrium and posture: head starts to tip toward as you fall asleep; muscles contract to raise the head) Very sudden muscle stretch causes tendon reflex - Knee jerk (patellar) reflex is monosynaptic reflex - Testing somatic reflexes helps diagnose many diseases Reciprocal inhibition prevents mucles from working against each other |
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Patellar Tendon Reflex |
1. Extensor muscle stretched 2. Muscle spindle stimulated 3. Primary afferent neuron excited 4. Primary afferent neuron stimulates alpha motor neuron to extensor muscle 5. Alpha motor neuron stimulates extensor muscle to contract 6. Primary afferent neuron stimulates inhibitory interneuron 7. Interneuron inhibits alpha motor neuron to flexor muscle 8. Flexor muscle (antagonist) relaxes Tapping the patellar ligament with a reflex hammer suddenly stretches the thigh muscle (muscle spindle detect muscle length and stretch). This stimulates numerous muscle spindles in the thigh and sends an intense volley of signals to the spinal cord, mainly by afferent fibers. (info carried to spinal cord by 1a afferent axon - 1a fiber is a proprioceptive afferent (carries info about deep somatic structures.) In the spinal cord, the primary afferent fibers (1a) synapse directly with the alpha motor neurons that innervate the muscle. -Monosynaptic reflex arc - only one synapse between the afferent and efferent neuron, so there's little synaptic delay and a very prompt response. The alpha motor neurons (1a) excite the thigh, making it contract and create the knee-jerk. Alpha motor neurons innervating the antagonist muscle are inhibited. |
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Flexor Withdrawal Reflexes |
-Occurs during withdrawal of foot from pain -Polysynaptic reflex arc (many synapses) -Neural circuitry in spinal cord controls sequence and duration of muscle contractions 1. Stepping on glass stimulates pain receptors in right foot 2. Sensory neuron activates multiple interneurons 3. Ipsilateral motor neurons to flexor excited 4. Ipsilateral flexor contracts 5. Contralateral motor neurons to extensor excited 6. Contralateral extensor contracts Stepping on a piece of glass: even before being consciously aware, you pull your foot away before the glass penetrates deeper. This action involved contraction of the flexor and relaxation of the extensors in the limb. Sustained contraction of the flexors is produced by parallel after-discharge circuit in the spinal cord. -Polysynaptic reflex arc: pathway which signals travels over many synapses on their way back to the muscle -Flexor muscles receive prolonged output from spinal cord until they die out Maintains balance by extending other leg Intersegmental reflex extends up and down the spinal cord Contralateral reflex arcs explained by pain at one foot causes muscle contraction in other leg |
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Golgi Tendon Reflex |
Proprioceptors in a tendon near its junction with a muscle - 1mm long, encapsulated nerve bundle Excessive tension on tendon inhibits motor neuron - Muscle contraction decreased Also functions when muscle contracts unevenly |
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3 Major Parts of the Brain |
-Cerebrum -Cerebellum -Brainstem |
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Cerebral hemisphere |
Longitudinal fissure: separates cerebral hemispheres Gyri are folds Sulci are grooves Cortex: surface layer of gray matter Nuclei: deeper masses of gray matter Tracts: bundles of axons (white matter) |
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Gray and White Matter |
Gray matter: the seat of neuron cell bodies, dendrites and synapses -- Dull, white color when fresh, due to little myelin -- Forms surface layer (cortex), over cerebrum and cerebellum -- Forms nuclei deep witghin brain White matter: bundles of axons -- Lies deep to cortical gray matter, opposite relationship in the spinal cord -- Pearly white color from myelin around nerve fibers -- Composed of tracts, or bundles of axons, that connect one part of the brain to another, and to the spinal cord |
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Cortical Localization: Central Gyrus |
Precentral gyrus: primary motor Postcentral gurys: sensory |
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Functions of Cerebral Lobes |
Frontal: voluntary motor functions, planning, mood, smell, and social judgement Parietal: receives and integrates sensory info Occipital: visual center of brain Temporal: areas for hearing, smell, learning, memory, emotional behavior (Superior gyrus: audition) |
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Brain Injuries |
Parietal lobe: -- Right hemisphere: contralateral neglect syndrome -- Left hemisphere (dominant hemisphere in 95% of people): Wenicke's aphasia - problems with comprehension of spoken language Temporal lobe (inferior occipitotemporal cortex): -- Inability to recognize objets (agnosia) or faces (prosopagnosia) Frontal lobe: problems with personality (inability to plan and execute appropriate behavior) |
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Phineas Gage |
In 1848, while tamping blasting powder for a railroad construction project, the tamping rod was blasted through Phineas' skull -This is the classic example of traumatic frontal lobotomy: ===> Ventromedial region of both frontal lobes: profound personality change; irreverent, profane, irresponsible ===> Prefrontal cortex function: planning, moral judgement, and emotional control |
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Emotion |
-Prefrontal cortex (seat of judgement): controls expression of emotions -Form in hypothalamus and amygdala (feelings themselves) : fear, anger, pleasure, love, etc. -Behavior: often learned by rewards and punishments or responses of others |
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Hippocampal Formation |
The hippocampus is within the temporal lobe, and is important for memory -Damage to the hippocampus can cause an inability to acquire new memories and may cause problems with retrieving old memories -Acetylcholine is an important neurotransmitter in the hypocampus |
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Alzheimer's Disease |
-Early stages: memory loss for recent events Pathophysiology - Cerebral autopsy - Neuronal loss in areas that connect with the hippocampus: cholinergic (ACh) neurons are lost -----> Aricept (donezepil) is a cholinesterase inhibitor (though it doesn't cure disease) -Amyloid plaques (beta amyloid) -Neurofibrillary tangles |
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Basal Ganglia |
Deep nuclei in the cerebral hemispheres -Most known function is to influence motor activity by modulating the cerebral cortex -Also influences cognitive and emotional functions Basal ganglia pathology manifests primarily as motor dysfunction |
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Parkinson's Disease |
Loss of dopamine, decreases thalamocortical excitation Characteristics: - Bradykinesis: slowness of movements, difficulty initiating movements - Rigidity: cogwheel type - Gait instability: festinating gait - trouble starting and stopping - Resting tremor: 4-6Hz, often pill-rolling - Masked face: smooth, expressionless Pharmacologial treatment with L-dopa, which unlike dopamine, crosses the BBB Loss of pigmentation in the substatia nigra is indicative of loss of dopaminergic neurons (Parkinson's) |
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Thalamus |
Oval mass of gray matter protrudes into lateral ventricle and 3rd ventricle of the brain It serves as a sensory relay region receiving nearly all sensory info on its way to cerebral cortex (except olfactory - smell) Relays signals from cerebellum to motor cortex |
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Hypothalamus |
Walls and floor of 3rd ventricle Functions: - Hormone secretion - Autonomic NS control - Thermoregulation - Food and water intake (hunger and satiety) - Sleep and circadian rhythms - Memory (mammillary bodies) - Emotional behavior |
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Reticular Formation |
-Loosely organized web of gray matter that runs vertically through all levels of the brainstem -Clusters of gray matter scattered throughout pons, midbrain, and medulla -Occupies space between white fiber tracts and brainstem nuclei -Has connections with many areas of cerebrum (More than 100 small neural networks without distinct boundaries) |
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Medulla Oblongata |
-Cardiac center: adjusts rate and force of heart -Vasomotor center: adjusts blood vessel diameter -Respiratory centers: control rate and depth of breathing -Reflex centers: for coughing, sneezing, gagging, swallowing, vomiting, salivation, sweating, movements of tongue and head |
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Cerebellar Disorders |
Cerebellar damage has ipsilateral consequences Signs: - Ataxia: uncoordinated, clumsy gait - Dystremia: abnormal overshoot/undershoot - Dysrythmia: abnormal rhythm and timing movements - Dysdiadochokinesia: pt cannot perform rapidly alternating movements |
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Blood Supply of the Brain |
The brain receives blood via 2 sources: - Vertebral arteries - Internal carotic arteries Problems arise when one of more of these vessels become occuded by atherosclerosis (hardness of arteries) |
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Stroke (cerebrovascular accident) (CVA) |
Sudden death (infarction) of brain tissue caused by ischemia -Cerebral ischemia can be produced by atherosclerosis, thrombosis, or a ruptured aneurysm ---> The effects of a stroke range from unnoticeable to fatal, depending on the extent of tissue damage and the function of the region of the brain that is damaged ---> Recovery depends on the ability of neighboring neurons to take over the lost function and on the extent of collateral circulation to regions of the brain |
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Transient Ischemic Attack (TIA) |
Characterized by temporary signs and symptoms of a stroke - The patient presents as if they are having a stroke but they fully recover function in minutes to several hours (They could have dizziness, loss of vision, weakness, paralysis, headache, aphasia) - TIA is strong predictor of future stroke if left untreated |
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Circle of Willis |
Forms at a base of the brain -It is an anastomosis (connection) between the vertebrobasilar (from the paired vertebral arteries) and internal carotid systems |
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Middle Cerebral Artery Stroke |
Causes contralateral hemiplegia (paralysis on opposite side) -Dominant hemisphere strokes affect speech and language -Non-dominant hemisphere (right hemisphere) stroke causes neglect syndrome (most often left neglect) |
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Blood-Brain Barrier (BBB) |
Important clinically - Permeable to lipid-soluble materials, alcohol, oxygen, carbon dioxide, nicotine and anesthetics - Diseases of the brain MUST be treated with drugs that can cross the BBB (in Parkinson's, dopamine is reduced - treatment with L-dopa, which is a precurson that can cross BBB, since dopamine cannot) |
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Meninges of the Brain: |
Dura Mater: Outermost, tough membrane - Outer periosteal layer against bone - Where separated from inner meningeal layer forms dural venous sinuses which drain blood from brain - Meningeal layer may fold inward to separate major parts of brain from each other (acts as supportive structure) : falx cerebri, falx cerebelli, and tentorium cerebelli - Epidural space filled with fat in low back (epidural anesthesia during childbirth) Arachnoid and Pia Mater: - Subarachnoid/subdural spaces |
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Meningitis |
-Inflammation of meninges -Bacterial or viral invasion of the CNS by way of the nose and throat -Signs include high fever, stiff neck, drowsiness, intense headache - may progress to coma -Diagnose is by examination of CSF (lumbar puncture - spinal tap) Treatments: - Bacterial: could be caused by one of a number of bacteria - IV antibiotics - Viral: usually resolves on its own unless severe |
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Epidural Bleed |
Dura mater has its own blood supply, separate from brain's Epidural hemorrhage is usually caused by trauma to the temple - Blood collects between the bone of the skull and the periosteal layer of dura - Slowly separates the periosteal dura from the bone EMERGENCY SITUATION! |
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Subdural Bleed |
Blood from torn veins fills the potential space between the dura and the arachnoid mater -Typically occurs in elderly pts ---> Brain is atrophied, so more space between brain and arachnoid ---> Puts strain on veins from brain to dural venous sinuses -Slow, insidious (with or without consciousness) |
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Ventricles |
Ventricles of the brain are internal chambers that are filled with CSF -Internal chambers within the CNS ----> Lateral ventricles in cerebral hemispheres ----> 3rd ventricle: single vertical space under corpus callosum ----> Cerebral aqueduct runs through midbrain ----> 4th ventricle: chamber between pons and cerebellum ----> Central canal runs down through spinal cord Lined with ependymal cells Choroid plexus produce CSF |
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Cerebrospinal Fluid (CSF) |
-CSF is clear liquid that fills ventricles and subarachnoid space -Brain produces and absorbs 500mL/day (choroid plexus creates CSF by filtration fo blood) -Functions: ---> Floats brain so it's neutrally buoyant ---> Cushions from hitting inside of skull ---> Chemical stability: rinses away wastes -Escapes (4th ventricle) to surround brain -Absorbed into venous sinus by arachnoid villi |
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BBB & Blood-CSF Barrier |
-BBB is endothelium (permeable to lipid-soluble materials, alcohol, etc.). ----> Circumventricular organs: in 3rd & 4th ventricles - blood has direct access (no BBB), which enable the brain to monitor and respond to fluctuations in blood glucose, pH, osmolarity, and other variables. It's also route for HIV virus to invade brain -Blood-CSF barrier at choroid plexus is ependymal cells joined by tight junctions |
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Hydrocephalus |
Abnormal accumulation of CSF in brain, usually from blockage of route of flow and reabsorption -Can be due to congenital obstruction of aqueduct of Sylvius -Tumors can block the aqueduct -In children, before skull sutures and is fused, the head swells -CSF expands the ventricles and compresses the NS -Hydrocephalus can severely damage brain tissue -Surgery can be performed, placing a shunt (tube) that drains the CSF into the neck or abdominal cavity |
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Limbic System |
Loop of cortical structures - Amygdala, hippocampus and cingulate guys Role in emotion and memory - Pleasure and aversion centers - Drugs of abuse primarily affect the limbic system (addiction) |
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Olfactory Nerve (I) |
Responsible for the sense of smell -Damage causes impaired senses of smell (anosmia) ----> Can be caused by occupational solvents (ex. acetone) |
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Optic Nerve (II) |
Provides vision -Damage causes blindness in visual field |
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Oculomotor Nerve (III) |
Controls eye movement, opening of eyelid, constriction of pupil, focusing -Damage causes drooping eyes (ptosis), dilated pupil, double vision, difficulty focusing and inability to move eye in certain directions |
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3rd Nerve Palsy |
Injury to the oculomotor nerve (III), causes: -Affected eye to look down and out (Unopposed action of the lateral rectus and superior oblique muscles) -Eyelid closed on affected side -Pupil is fixed and dilated |
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Trochlear Nerve (IV) |
Controls one muscle of eye movement (superior oblique muscle) -Damage causes double vision and inability to rotate eye inferior-laterally |
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4th Nerve Palsy |
Trochlear palsy: - Affected eye looks upward when pt asked to stare ahead - Pt suffers from diplopia (double vision) - Pt tilts head downward away from affected eye to compensate |
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Trigeminal Nerve (V) |
Provides sensory innervation to face (touch, pain and temperature) and muscles of mastication -Damage produces loss of sensation and impaired chewing |
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Trigeminal Neuralgia |
(a.k.a tic douloreux) -Most common cranial neuralgia -Characterized by attacks of excruciating pain over the distribution of one or more of the branches of the trigeminal nerve -Carbazepime, is regarded by most as the medical treatment of choice. Stabilizes inactivated Na+ channels. |
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Abducens Nerve (VI) |
Provides eye movement via lateral rectus muscle -Damage results in inability to gaze laterally |
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6th Nerve Palsy |
Injury of the abducens nerve causes a lateral gaze deficit -Can't look sideways, affected eye does not move past the midline of the orbit |
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Facial Nerve (VII) |
Innervates the muscles of facial expression, salivary glands and tear, nasal and palantine glands. It provides a sensory taste on anterior 2/3 of tongue -Damage produces sagging facial muscles and disturbed sense of taste --> Clinical test: test anterior 2/3s of tongue with substances like sugar, salt, vinegar, and quinine; test response of tear glands to ammonia fumes; test motor functions by asking pt to close eyes, smile, whistle, frown, raise eyebrows |
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Bell's Palsy |
Most common facial nerve disorder -Sudden weakness in muscles on one half of face (sag) -Spontaneous onset over hours or days -Gradual recovery usually follows -Unknown cause (may be viral or inflammatory) -About 80% of pts recover in 3 weeks -Treatments include corticosteroid anti-inflammatory drugs - Antiviral drug acyclovir is used too, but not very effient |
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Vestibulocochlear Nerve (VIII) |
Innervates structures that provide hearing and sense of balance -Damage produces deafness, dizziness, nausea, loss of balance and nystagmus (eyes vibrate from side to side) -Some pharmaceuticals are ototoxic (aspirin and some antibiotics). They irreparably damage hair cells in the cochlea (inner ear organ for hearing) |
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Acoustic Neuroma (Acoustic Schwannoma) |
-Slow growth (years) -Benign tumor, but space occupying -Tinnitus (ringing in ears), hearing loss and vertigo (dizziness), but may cause facial paralysis because of compression of facial nerve |
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Glossopharyngeal Nerve (IX) |
Controls swallowing, salivation, gagging, controls blood pressure and respiration. Sensation from posterior 1/3 of tongue -Damage results in loss of bitter and sour taste and impaired swallowing |
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Vagus Nerve (X) |
Swallowing, speech, regulation of viscera (slows heart rate, and promotes peristalsis of gut) -Damage causes hoarseness or loss of voice, impaired swallowing and fatal if both are cut |
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Deviation of Uvula |
When there's an injury to Vagus Nerve (X), on examination of the oral cavity, the uvula will deviate to the opposite (normal) side Also, the palatoglossus muscle, a muscle which elevates the lateral margin of the tongue, will not contract on the affected side |
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Accessory Nerve (XI) |
Innervates 2 muscles that control head, neck and shoulder movement -Damage causes impaired head, neck, shoulder movement; head turns toward injured side (trapezius atrophy and shoulder droop) |
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Hypoglossal Nerve (XII) |
Controls tongue movements for speech, food manipulation and swallowing -If both are damaged: can't protrude tongue -If one side is damaged: tongue deviates towards injured side (ipsilateral atrophy) |
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Hypoglossal Nerve Injury |
Because of the actions of the tongue muscles, an injury to the hypoglossal nerve causes the protruded tongue to point toward the side of the nerve injury |
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General Properties of the Autonomic Nervous System (ANS) |
ANS (a.k.a. visceral motor system) is a set of efferent pathways from the CNS that innervates: - smooth muscle - cardiac muscle - glands -Regulates unconscious processes that maintain homeostasis (BP, body temperature, respiratory airflow) |
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Visceral Reflexes |
Unconscious, automatic responses to stimulation of glands, cardiac or smooth muscle 1. Receptors: detect internal stimuli (stretch, blood chemicals, etc.) 2. Afferent Neurons: connect to interneurons in the CNS 3. Efferent Neurons: carry motor signals to effectors (ANS is the efferent neurons of these reflex arcs) 4. Effectors: glands, smooth or cardiac muscle -ANS modifies effector activity |
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Visceral Reflex to High Blood Pressure |
High Blood Pressure: - Is detected by arterial stretch receptors called baroreceptors(1), - Afferent neuron in glossopharyngeal nerve carries signal to medulla (CNS) (2) - Vagus nerve (efferent) signals travel to the heart (3) - Heart slows, which reduces blood pressure (4) |
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Autonomic Pathways |
In autonomic pathways the signal must travel across 2 neurons to get to the target organ, and it must cross a synapse where these 2 neurons meet in an autonomic ganglion -The 1st neuron, called preganglionic neuron has a soma in the brainstem or spinal cord (its axon terminates in the ganglion) - The 1st neuron synapses with the postganglionic neuron whose axon extends the rest of the way to the target cells |
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Divisions of the ANS |
Two divisions (sympathetic & parasympathetic) innervate the same target organs in most cases (may have cooperative or contrasting effects) 1. Sympathetic division: prepares body for physical activity ("fight or flight") ---> Increases heart rate, BP, pulmonary airflow, blood glucose levels, blood flow, to cardiac and skeletal muscles (while reducing blood flow to skin and digestive tract) 2. Parasympathetic division: calms many body functions and assists in bodily maintenance ("rest and digest") - digestion and waste elimination Many resources refer to a 3rd division of the ANS called the enteric nervous system, which resides within the GI tract |
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Autonomic Tone |
The background rate of activity of the ANS -It is the balance between the sympathetic and parasympathetic tone ---> Parasympathetic tone maintains smooth muscle tone in the intestines and holds the resting heart rate down to about 70-80 beats/minute ---> If the parasympathetic Vagus nerves to the heart are cut, the heart beats at its own intrinsic rate of about 100 beats/minute ----> Sympathetic tone keeps most blood vessels partially constricted and thus maintains blood pressure (loss of sympathetic tone can cause such a rapid drop in BP that a person goes into shock) |
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Organization of the ANS |
Synapses between neurons are made in autonomic ganglia - Sympathetic ganglia are located in the paravertebral chain (or prevertebral) - Parasympathetic ganglia are located in or near the effector organ |
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Sympathetic NS Overview |
- Presynaptic (preganglionic) neurons have their cells bodies in the lateral horns of spinal cord (T1-L2) thoracolumbar -Sympathetic chain ganglia (paravertebral) ----> Cervical, thoracic, lumbar, sacral, and coccygeal ganglia ----> White and gray communicating rami suspend ganglia from spinal nerve ----> Pathways of preganglionic fibers: --------- 1. Enter ganglia and synapse on postganglionic cell --------- 2. Travel to higher or lower ganglia and synapse --------- 3. Pass through chain without synapsing to reach collateral ganglia via splanchnic nerves Neuronal cell bodies of the intermediolateral cell column (T1-L2) axons leave the spinal cord via ventral roots. They are the sympathetic preganglion neurons and they use Ach when they synapse in ganglia |
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Somatic vs. Autonomic Pathways |
Motor (Efferent): from CNS to effector Somatic efferent innervation: signal travels from spinal cord through axons (myelinated neuron fibers) directly to skeletal muscles (somatic effector) Autonomic efferent innervation: signal travels from spinal cord through presynaptic neuron ( myelinated preganglionic fiber) cell, releases a neurotransmitter at the autonomic ganglion region, which synapses on unmyelinsted postganglionic cell (postsynaptic neuron) and synapses (2nd neurotransmitter) reaching the visceral effector (cardiac muscle, smooth muscle, or glands) - Uses 2 neurons (presynaptic and postsynaptic) and neurotransmitters |
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Sympathetic Pathway May: |
As axons leave the intermediolateral cell column and enter the sympathetic chain, they may do one of four things: 1. They may ascend in the chain and synapse in more superior ganglia 2. They may descend in the chain and synapse in more caudal ganglia 3. They may pass through the chain without synapsing and go to a prevertebral ganglion 4. They may synapse in the ganglion at the same spinal level from which they arose -Preganglionic sympathetic neurons arise from the troracolumbar (T1-L2) spinal cord segments |
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Neuronal Divergence & Convergence |
Neuronal divergence is present in sympathetic system - Each preganglionic cell branches and synapses on multiple (10-20) postganglionic cells - Produces widespread effects on multiple organs Neuronal convergence is also present - Each postganglionic may receive synapses from multiple preganglionic neurons |
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Adrenal Glands |
Sympathoadrenal system is the closely related functioning adrenal medulla and sympathetic NS - Adrenal (suprarenal) glands sit on superior pole of each kidney (Adrenal cortex secretes steroid hormones and androgens - endocrine gland) Adrenal Medulla (inner core) - Is a modified sympathetic ganglion (stimulated by preganglionic sympathetic neurons that send fibers that penetrate the cortex of the gland and terminate on the chromaffin cells of the adrenal medulla) - Chromaffin cells of the adrenal medulla secrete neurotransmitters (hormones) into blood -----> Catecholamines (85% epinephrine, 15% norepinephrine, and a trace of dopamine) |
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Sympathetic Innervation |
Effectors in body wall (sweat glands, blood vessels, erector pilli muscle) are innervated by sympathetic fibers that travel in spinal nerves Effectors in head and thoracic cavity are innervated by fibers in sympathetic nerves that for the most part travel with blood vessels to reach their targets Effectors in abdominal cavity are innervated by sympathetic fibers in splanchnic nerves (Celiac, superior, and inferior mesenteric ganglion) There are about 17 postganglionic neurons for every preganglionic neuron in the sympathetic division ---> This means that when one preganglionic neuron fires, it can excite multiple postganglionic fibers leading to different target organs. Thus the sympathetic division tends to have widespread effects |
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Sympathetic NS Summary |
Preganglionic neurons: - In the spinal cord lateral horn fromT1-L2 or 3 - Some synapse in paravertebral ganglia -- Others travel via splanchnic nerves to prevertebral ganglia, or directly to the adrenal medulla - Cholinergic (acetylcholine) Postganglionic neurons: - In paravertebral (sympathetic chain) or some prevertebral (collateral) ganglia - Most are adrenergic (epinephrine or norepinephrine) -----> Exception: Merocrine (cooling) sweat glands use ACh |
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Parasympathetic NS Divergence |
There is some neural divergence in the parasympathetic division, but much less than in the sympathetic -Has a ration of fewer than 5 postganglionic fibers to every preganglionic fiber - The long preganglionic fiber reaches the target organ before the slight divergence occurs - The parasympathetic NS is thus relatively selective in its stimulation of target organs as compared to the sympathetic |
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Parasympathetic NS Pathways |
Cranial nerves III, VII, IX are responsible for parasympathetics to the head Cranial nerve X and sacral spinal cord segments are responsible for parasympathetics of all viscera of the body cavities |
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Parasympathetic (Craniosacral) NS |
Origin of preganglionic fibers - Brain stem for cranial nerve nuclei - Sacral spinal cord segments S2-S4 Pathways of preganglionic fibers - They leave the brain stem in the cranial nerves (III, VII, IX, X) - They also arise from sacral spinal cord Terminal ganglia in/near target organs - Long preganglionic, short postganglioci fibers |
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Parasympathetic Oculomotor Nerve (III) |
Cranial nerve III sends preganglionic axons to the Ciliary ganglion (Ach), postganglionic stimulates via (Ach) the pupillary constrictor and the ciliary muscle, which thickens lens for near vision |
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Parasympathetic Facial Nerve (VII) |
- Sends axons to the pterygpalatine (sphenopalatine) ganglion (Ach), which sends postganglionic axons (Ach) to lacrimal glands (tears), and nasal glands (mucus) - Sends axons to the submandibular ganglion (Ach), which sends postganglionic axons (Ach) to the sublingual and submandibular salivary glands |
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Parasympathetic Glossopharyngeal Nerve (IX) |
Sends axons to the otic ganglion (Ach), which sends postganglionic axons to the parotid salivary gland |
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Parasympathetic Vagus Nerve (X) |
-Viscera as far as proximal 2/3 of colon -Cardiac, pulmonary, and esophageal plexus |
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Enteric NS |
-NS of the digestive tract ---> Composed of 100 million neurons found in the walls of the digestive tract (no components in CNS) ---> Has its own reflex arcs: Regulates motility of esophagus, stomach, and intestines, and secretion of digestive enzymes and acid (also requiring regulation by the ANS) |
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Megacolon (Hirschsprung Disease) |
Hereditary defect causing absence of enteric NS - No innervation in sigmoid colon and rectum - Constricts permanently and will not allow passage of feces - Feces becomes impacted above constriction - Megacolon: massive dilation of bowel accompanied by abdominal distension and chronic constipation - May be colonic gangrene, perforation of bowel, and peritonitis - Usually evident in newborns who fail to have their first bowel movement |
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ANS Neurotransmitters |
- Cholinergic fibers which secrete Ach - Adrenergic fibers which secrete norepinephrine |
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ANS: Neurotransmitters and Receptors |
Effects on ANS: - Are determined by the types of neurotransmitters released and type of receptors on target cells Substances other than Ach and norepinephrine are released by neurons of the ANS: - Peptidergic neurons release peptides such as substance P (pain), neuropeptide Y (appetite) - Nitric oxide (NO) is released (NO inhibits muscle tone in blood vessel walls causing vasodilation) |
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Sympathetic Adrenergic |
Sympathetic has longer lasting effects - The norepinephrine released by sympathetic postganglionic nerve fibers is: ------> Reabsorbed by the nerve fiber where it's reused or broken down by Monamine oxidase (MAO) -------> Some diffuses into the surrounding tissues where it's degraded by another enzyme catechol-O-methyltransferase (COMT) ------> Much of it is picked up by the blood stream where MAO and COMT are absent - This norepinephrine along with epinephrine from the adrenal gland circulates throughout the body and exerts a prolonged effect |
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Nicotinic Receptors |
Nicotinic Ach receptors at ganglia: - Always excitatory - Receptors open ligand gated ion channels |
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Adrenergic Receptors for Norepinephrine |
Norepinephrine binds to 2 classes of receptors: - Alpha adrenergic receptors - Beta adrenergic receptors - Existence of subclasses of each receptor type: Alpha 1 and 2; Beta 1 and 2 (all 4 types function by means of second messengers) |
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Adrenergic Receptors (Alpha 1) |
Alpha 1: -Found on vascular smooth muscle of the skin and viscera, GI and bladder sphinchters, and radial of the iris - Produce excitation (contraction or constriction) - Mechanism of Action: Inositol triphosphate (IP3) and increase in intracellular calcium ion concentration ---> Phenylephrine is an agonist (sympathomimetic) - used as decongestant |
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Adrenergic Receptors (Alpha 2) |
- Found in platelets, fat cells, and walls of GI tract - Often produce inhibition (relaxation and dilation) - Mechanism of Action: inhibition of adenylate cyclase and decrease in cAMP ---> Clonidine is agonist ---> Yohimbine is antagonist |
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Adrenergic Receptors (Beta 1 & 2) |
Mechanism of Action: activation of adenylate cyclase and production of cAMP ---> Propanolol is antagonist (B-adrenergic blocker - nonselective) Beta 1: - SA node, AV node, and ventricular muscle of heart - Produce excitation (increase heart rate, conduction velocity, increased contractility) Beta 2: - Vascular smooth muscle in skeletal muscles, bronchial smooth muscle, smooth muscle in wall of GI tract, bladder - Produce relaxation (dilation of vascular smooth muscle and bronchioles, relaxation of bladder wall) - Albuterol is selective B2 antagonist (sympathomimetic) |
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Cholinergic Receptors |
Acetylchonic (Ach) binds to 2 classes of receptors: - Nicotinic receptors - Muscarinic receptors |
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Nicotinic Cholinergic Receptors |
-Activated by Ach and nicotine -Located in all autonomic ganglia (sympathetic and parasympathetic), in adrenal medulla, and at NMJ of skeletal muscle ----> Receptors are similar but not identical in these locations - Mechanism of Action: Ach binds to alpha subunits of the nicotinic Ach receptor, which are also ion channels for Na+ and K+ -----> Excitatory when Ach binding occurs -----> Curare binds selectively to nicotinic receptors |
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Muscarinic Cholinergic Receptors |
-Located on all heart, smooth muscle, and glands (except vascular smooth muscle) -Excitatory or inhibitory due to subclasses of muscarinic receptors ---> Inhibitory in the heart: decrease heart rate, decrease conduction velocity in AV node -----> Mechanism of Action: inhibition of adenylate cyclase, which leads to opening of K+ channels - slowing spontaneous depolarization -Excitatory in smooth muscle and glands: ----> Increased GI motility and increase secretion ----> Mechanism of Action: formation of Inositol triphosphate (IP3) and increase in intracellular calcium Muscarinic receptors are blocked by Atropine |
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Muscarinic Receptors |
Five major subclasses: The heart is mostly M2 - Inhibitory receptor (reduces cAMP) Most glands & smooth muscle have M3 - Excitatory (increases calcium) M1, M4, and M5 are mostly in CNS |
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Dual Innervation |
-Most of viscera receive nerve fibers from both parasympathetic and sympathetic divisions -Both divisions do not normally innervate an organ equally Antagonistic effects (oppose each other) - Can be exerted through dual innvervation of same effector ---> Heart rate decreases (parasympathetic), hate rate increases (sympathetic) ---> Sympathetic inhibits digestion and parasympathetic stimulates it Can be exerted because each division innervates different cells - Pupillary dilator muscle (sympathetic) dilates pupil, constrictor pupillae (parasympathetic) constrict pupil ----> Preganglionic sympathetics in CN III, oculomotor synapse in ciliary ganglion with postganglionic neurons that innervate constrictor pupillae -Cooperative effects seen when 2 divisions act on different effectors to produce unified effect ---> Parasympathetics increase salivary serous cell secretion (watery and enzyme-rich), sympathetics increase salivary mucous cell secretion (thick and rich in mucous) |
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Control Without Dual Innervation |
Some effectors receive only sympathetic (Adrenal medulla, arrector pili muscles, sweat glands and many blood vessels)
Sympathetic tone: -A baseline firing frequency -Vasomotor tone provides partial constriction ---> Increase in firing frequency causes vasoconstriction ---> Decrease in firing frequency causes vasodilation -Can shift blood flow from one organ to another as needed ---> Sympathetic stimulation increases blood to skeletal and cardiac muscles - reduced blood to skin in times of emergency or stress or exercise =====> Temporary diversion of blood to where it's needed most =====> Digestion, nutrient absorption, and urine formation can wait thus sympathetic division constricts arteries to the GI tract and kidneys |
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Sympathetic and Vasomotor Tone |
Vasoconstriction: (1)Strong sympathetic tone; (2)Smooth muscle contraction; (3)Vasoconstriction Vasodilation: (1)Weaker sympathetic tone; (2)Smooth muscle relaxation; (3)Blood pressure dilates vessel -Sympathetic division prioritizes blood vessels to skeletal muscles and heart in times of emergency (Beta 2 receptors) -Blood vessels to skin vasoconstrict to minimize bleeding if injury occurs during stress or exercise (Alpha 1 receptors) |
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Central Control of Autonomic Function |
ANS regulated by several levels of CNS: -Cerebral cortex: anger, fear, thoughts of food, sex, anxiety - limbic system connects sensory and mental experiences with ANS -Hypothalamus (major visceral motor control center): nuclei for cardiac and vasomotor control, salivation, swallowing, sweating, bladder control, and pupillary changes -Spinal cord reflexes: defecation and micturition reflexes integrated in spinal cord - brain can inhibit these responses consciously |
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Drugs (Sympathetics) |
Sympathomimetics enhance sympathetic activity - Stimulate receptors or increase norepinephrine release ----> Phenylephrine in cold remedies: stimulate alpha 1 receptors dilating bronchioles and constricting nasal blood vessels to reduce swelling in nasal mucosa allowing ease of breathing (decongestant) Sympatholytics suppress sympathetic activity - Block receptors or inhibit norepinephrine release ----> Propanolol is a beta-blocker that reduces hypertension by blocking beta adrenergic receptors on heart and blood vessels |
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Drugs (Parasympathetics) |
Parasympathomimetics -Enhance parasympathathetic acitivity ---> Pilocarpine relieves glaucoma (excessive pressure in eyeball) by contracting iris sphincter (miosis) facilitates dilating aqueous humor outflow into blood vessels that drain fluid from the eye Parasumpatholytics -Suppress parasympathetic activity ---> Ganglionic, neuromuscular (nicotinic cholinergic) ---> M1 through M5 (muscarinic cholinergic) : Atropine blocks muscarinic receptors and is sometimes used to dilate pupils for eye examination and to dry mucous membranes of respiratory tract before inhalation anesthesia |
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Sympathetic NS Summary |
"Fight or Flight" - Defense System -Increased arterial pressure -Increased heart rate and contractility -Increased blood flow to skeletal muscles -Decreased blood flow to GI tract -Increased cellular metabolism -Increased glycolysis and blood glucose -Increased pupil diameter/lens flattening |
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Parasympathetic NS Summary |
"Rest and Digest" -Miosis (pupillary constriction) -Bradycardia, bronchoconstriction -Lacrimation (tearing) -Urination -Erection -Salivary, GI secretions and motility -Defecation |
