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66 Cards in this Set

  • Front
  • Back

smaller motor units

-fewer fibers


-recruited first


-slow-twitch oxidative


-contract and relax slowly


-contribute less force

larger motor units

-more fibers


-recruited later


-fast-twitch glycolytic


-contract and relax quickly


-contribute more force

soleus

posture muscle

activation of autonomic division

-pupillary dilation


-adrenaline rush


-increased heart rate


-increased blood pressure

sympathetic system

"fight-or-flight"


energetic

parasympathetic

"rest-and-digest"


restorative

main characteristics of autonomic motor division

-dual antagonistic input to target tissues


-diffuse release of NT on target tissue


-typically involuntary


-homeostatic

mechanistic themes for maintaining homeostasis in autonomic division

-dual antagonistic control


-tonic control


-variable receptor expression

hypothalamus

synthesizes and secretes certain neurohormones which control body temperature, hunger, thirst, fatigue, sleep, and circadian rhythms

medulla

functions of breathing, heart rate and blood pressure

pons

sleep, respiration, swallowing, bladder control, hearing, equilibrium, taste, eye movement, facial expressions, facial sensation, and posture

main autonomic control regions

hypothalamus


medulla


pons

dorsal root

sensory input enters here

ventral root

somatic input exits here

ganglion

collection of cell bodies and tissues

general organization of autonomic motor neurons

-two efferent neurons


-first neuron is in the CNS


-second neuron is in the PNS (autonomic ganglia)

distribution of parasympathetic ganglia

exit CNS at brainstem and sacral (bottom of spinal cord)

distribution of sympathetic ganglia

near spinal column


thoracic and lumbar (mid spinal cord)

parasympathetic axons

preganglionic axons arise from cranial nerves and S2-S4 spinal nerves


vagus nerve contains 75% of all parasympathetic fibers

sympathetic axons

preganglionic axons arise from T1-L2 spinal nerves

sympathetic neurotransmitters

preganglionic neuron releases ACh which binds to nicotinic receptor on autonomic receptor


this releases norepinephrine to an adrenergic receptor on target tissue

metabotropic

GPCR pathway

adrenergic

metabotropic pathway for norepinephrine and epinephrine

cholinergic

pathway for acetylcholine

nicotinic

cholinergic ionotropic pathway

muscarinic

cholinergic metabotropic

varicosities

chain of release sites for neurotransmitters

release of norepinephrine from varicosity to target cell

1. action potential arrives at varicosity


2. depolarization opens voltage-gated Ca channels


3. Ca entry triggers exocytosis of synaptic vesicles


4. NE binds to adrenergic receptor on targets


5. Receptor activation ceases when NE diffuses away from the synapse


6. NE is removed from synapse


7. NE can be taken back into synaptic vesicles for re-release


8. NE is metabolized by monoamine oxidase (MAO)

cholinergic synapses

parasympathetic varicosity releases acetylcholine to a muscarinic receptor which activates an amplifier enzyme and ACh is removed by AChE

adrenergic synapses

sympathetic varicosity releases nor/epinephrine to an adrenergic receptor which activates an amplifier enzyme and is removed from monoamine transporter (MAT)



parasympathetic responses

pupil constriction, slow heart rate, lung constriction, increased digestion, bladder release, erection

sympathetic responses

pupil dilation, fast heart rate, lung dilation, decreased digestion, bladder retention, skin vessel constriction, muscle vessel dilation, ejaculation

cocaine

-indirect agonist


-blocks reuptake of NE into adrenergic nerve axon terminals by binding membrane transporter or uptake site


-extends NE's excitatory effect on target


-"upper"

anti-depressants

-indirect agonists that act on membrane transporters (SSRIs)


-prevention of degradation (MAOIs)

side effects of MAOIs

-heart problems


-constipation and urination difficulty


-sexual dysfunction

iris sphincter

constricts eye, parasympathetic, muscarinic ACh receptors

iris dilator

dilates eye, sympathetic, α1 adrenergic cause contraction

sympathetic response is dominant when

sympathetic response is enhanced OR parasympathetic response is inhibited

parasympathetic response is dominant when

parasympathetic response is enhanced OR sympathetic response is inhibited

atropine

dilating drug: mydriatic


muscarinic antagonist blocks the muscarinic ACh receptor


"parasympatholytic" drug

phenylephrine

dilating drug: mydriatic


adrenergic agonist stimulates α1 adrenergic receptors


"sympathomimetic" drug

chromaffin cells

make up adrenal medulla


secrete 80% epinephrine and 20% norepinephrine

multiunit smooth muscles

blood vessels

resting tonic control

sympathetic release of norepinephrine to arteriole/vein

constriction of arteriole/vein

more NE released to arteriole/vein, α1 receptor (intestine/skin)

dilation of arteriole/vein

less NE released to arteriole/vein

epinephrine receptor

B2 receptor, vessel dilates (skeletal muscle)

phosphorylation

transfer of a phosphate group

dephosphorylation

removal of a phosphate group

why have different receptors that respond to the same set of ligands?

fine control of local physiological responses, even with systematic release of hormone

smooth muscle lining BV of intestine/skin

more α1 adrenergic receptors, more norepinephrine

smooth muscle lining BV of skeletal muscle/bronchi

more B2 adrenergic receptors, more epinephrine

calcium initiates contraction

1. intracellular Ca concentration increases when Ca enters cell and is released from SR


2. Ca binds to calmodulin in cytosol


3. Ca-calmodulin activates myosin light chain kinase


4. MLCK phosphorylates light chains in myosin heads and increases myosin ATPase activity


5. active myosin crossbridges slide along actin and create muscle tension

calcium desensitization

increase in MLCP activity overrides increases in Ca

smooth muscle relaxation

ratio of MLCK: MLCP, MLCK dependent on Ca-CaM


1. free Ca in cytosol decreases when Ca is pumped out of cell or back into SR


2. Ca unbinds from CaM (MLCK activity decreases)


3. myosin phosphatase removes phosphate from MLC which decreases myosin ATPase activity


4. less muscle ATPase activity results in decreased muscle tension

Calcium entry to cytosol from ECF

voltage-gated Ca channels open in response to depolarizing stimulus


ligand-gated Ca channels open in response to ligand binding


stretch-activated channels open in response to change in muscle tone

Calcium-induced calcium release

RyR on SR open in response to small amounts of Ca entering from ECF


IP3 channels on SR open through adrenergic receptor activation

α1 adrenergic receptor

affinity for norepinephrine, only needs Ca from SR to cause contraction


activates PLC -> IP3 -> releases Ca from SR -> activates MLCK via Ca-CaM dependent kinase

B2 AR

affinity for epinephrine, causes relaxation


activates adenylyl cylase -> cAMP -> PKA -> phosphorylates MLCK


ALSO


inhibits IP3 binding to receptor


enhances Ca-ATPase activity at SR membrane


enhances MLCP activity

α2 AR

promotes contraction by inhibiting adenylyl cyclase

anaphylaxis

systematic allergic reaction


-respiratory distress


-hypotension


-hives


immediately inject epinephrine

epi-pen

α1 receptor prevents and relieves hypotension and shock & relieves upper airway obstruction


B2 receptor decreases wheezing and decreases hives

asthma

airway constriction and excess mucous secretion


histamine release triggered by allergens or airway irritants; smooth muscle of airway constricts in response to histamine

treatment for asthma

albuterol which dilates lung air passages

electromechanical coupling


depolarization can cause contraction

intracellular Ca conc increase when Ca enters cell and is released from SR

pharmomechanical coupling


ligand-binding causes contraction

IP3 induced calcium release