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106 Cards in this Set
- Front
- Back
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resting membrane potential
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- potential - a seperation of charge, in this case across a membrane.
units are volts - ability to do work - move ions and change a proteins concentration. |
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resting membrane potential
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- diff. in charge between inside and outside of cell
- electrochemical because it involves seperation of ions. - the inside of the cell is usually negative. - RMP is in steady state; energy is required to maintain it. |
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depolarization
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- a change in membrane potential so that it is closer to zero.
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hyperpolaraization
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- change in membrane potential so that it is farther from zero
- current - movement of charge - units are amperes - movement of Na, K and Ca |
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resting membrane potential terms
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- resistance - opposition to flow and the units are ohms
- ohm's law - relates voltage current and resistance V = IR - a current flowing through a resistance results in a potential. permeability - the ease with which an ion moves through an open channel - if a channel is open it has a permeability - ions to dont need to be present for a channel to have permeability. - conductance - - the amount of current a channel is carrying under given conditions and units are siemens conductance is th inverse of resistance g = 1/R - to have a conductance across a biological membrane there must be both permeability and permeant ions - therefore ions must be present to have conductance. |
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basis of the resting membrane potential
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- the distribution of certain ions across the membrane
- the membrane permeabilities of certain ions. - the na/k atpase - direct and indirect roles - The Na/k atpase - creates Na gradient to drive most types of secondary active transport - pumps 3 na out and 2 k in per each cycle (each ATP) - electrogenic - creates outward flow of cations - 2 roles in the resting membrane potential - indirect - establishes and maintains Na and K concentration gradients - direct - generates and electrical current that contributes about 10mV to teh RMP. - electrical vs. chemical potentials - electrical potential - difference in charge across the membrane (due to all ions) - chemical potential - difference in concentration of a given ion across the membrane (with respect to one ion) |
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equilibrium potential
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the membrane potential (voltage) at which no net flux of an ion occurs (electrical and chemical gradients)
- the nernst equation. - also called the reversal potential because it is the voltage at which flux of an ion changes directions |
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ion permeability
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- increaseing the membrane permeability of part. ion will drive the membrane potential towards the EP of that ion.
- effect of K ion movement on membrane potential - K+ exits the cell down its concentration gradient, but this is opposed by the electrical gradient. - Effect of K ion movement on membrane potential - K exits the cell down its conc. gradient, but this is opposed by the electrical gradient - Ek is ~ 90 mV vs. Em of ~ 70 mV ... Resting K+ permeability is relatively high, so Em is close Ek |
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resting membrane potential
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- effect of sodium ion movement on membrane potential -
- na enters teh cell down its conc. and electrical gradient. - Ena is ~60 mV vs. Em of ~70 mV - resting Na permeability is low, so Em is far from Ena |
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sumary of resting membrane potential
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- the Na/k atpase establishes conc. gradients for Na and K.
1. resting permeability to K>>Na - K flows out of the cell down its conc. gradient and stops when it is balanced by the electrical gradient. - a small amount of Na flows into the cell to slightly depolarize it. - the smaller teh na permeability the closer Em will be to Ek 2. large, impermeant anionic proteins inside the cell are very minor contributors 3. electrogenic activity of the Na/k atpase adds ~ 10 mV. |
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cell types in the CNS
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neurons - transmit and store info.
- functional unit of the CNS - communicate mainly via chemical synapses - glia - supporting cells - astrocytes - supply nutrients, buffer the ec environment, provide electrical insulation - principle cells responsible for scar formation and repair. - may also play an active role in signalling. - oligodendrocytes - form myelin sheaths around axons - microglia - form th macrophage of CNS, remove damaged cells and waste, release cytokines. - ependymal cells - line the ventricle of CNS. |
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cell types in cns cont.
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- gray vs. white matter - gray matter - cell bodies of neurons and glia
- white matter - myelinated axons - structure of a neuron - dendrites - soma - cell body - axon hillock - site of AP initiation. - myelin - insulating sheath - axon terminal - releases NT. |
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impulse production
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- graded potentials - local changes at sensory receptors at post synaptic side of synapse.
- occur at synapses, sensory receptors - local, short distance changes in membrane potential - variable in amplitude - stronger stimuli give larger amplitudes - passive conduction - like electricity in a wire - amplitude decreases with increasing distance. |
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action potentials
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- occur in excitable cells 9neurons and muscle cells)
- can travel long distances - all or none - ap amplitude is the same for any stimulus above threshold - active propagation - regenerates along the axon, so its amplitude is the same as it travels. - threshold potential - - membrane potential at which ap fires - occurs when gNa+>gK+ - |
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events of the ap
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- threshold - point at which gna>gk
- rising phase - rapid opening of the Na channels - overshoot - hyperpolarization -peak - Na channels maximally open; begin to inactivate -repolarization - K+ channels open - afterhyperpolarization - gk>gK at rest. |
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ion channels and the action potential
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- Na channels
- pen rapidly when depolarized - then inactivate - rapid and lasts unitl repolarized; distinct from closing. K channels - delayed rectifier - open slowly when depolarized - do NOT inactivate - close slowly. |
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refractory period
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- ap can only occur at a certain rate
- absolute refractory period - no additional AP's will fire - Na channels are inactivated relative refractory period - higher threshold for AP firing - more K+ channels are open compared to the resting state - AP peak is depressed due to a higher number of K+ channels. |
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ap propagation in unmyelinated axons
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- one area depolarizes to threshold, causing AP
- AP depolarizes adjacent area - regions become passively depolarized by AP , local graded potential, it is the wave that moves ahead - AP doesn't go backwards, previous area is refractory. |
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AP propagation on myelinated axons
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- impulse goes passively through myelin covered sections, actively through nodes
- passive conductions (like electricity through a wire) is much more rapid than active. |
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conduction velocity of diff. neurons
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- myelinated axons
- some sensory neurons (touch, proprioceptors) - motor neurons - need to be fast - velocity: few m/s to 100 m/s (225 mph) - unmyelinated figures - pain fibers - autonomic motor neurons to GI tract don't need to be fast. - velocity is .5-10 m/s (22.5 mph) - effect of size on conduction velocity - the larger the diameter, the faster the conduction velocity. - larger diameter - increased conduction velocity due to increased internal longitudinal resistance. |
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electrical synapses (gap junctions)
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cell types
- neuron to neuron (rare) - glia to glia ( more common) structure - each protein; connexin - group of 6 connexins: connexon - large channels that let things like nucleotide, proteins or sugars through. - connexons in adjacent cells connect to form a channel Ion Channel - non specific and constitutively active always and opening and closing or open all the time. - allows ions to flow between adjacent cells so that depolarization can spread (can shut down to pretect cell from damage) |
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chemical synapse
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major type of synapse in the nervous system
1. action potential depolarizes terminal opening Ca 2+ channels 2. Ca 2+ influx causes vesicles to fuse with membranes 3. vesicles release transmitter into cleft 4. transmitter binds to receptors on postsynaptic cell and either opens ion channels or alters 2nd messenger system. 5. action of transmitters is terminated. |
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synapse types
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- axodendritic - classical axon to dendrite
- axospinous - axon to dendritic spine; one o the most important in ns funciton and can change shape or NT fast - axosomatic - axon to cell body greater influce because it's closer to axon hilock. - axoaxonic - axon to another axon; often inhibitory; act to modulate release of transmitter (presynaptic modulation) - increase or decrease NT release. |
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synaptic potentials
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- graded potentials in the post synaptic neuron
- excitatory - transmitter increases the probability of AP firing (causes depolarization) - can involve Na or Ca channel opening or K channel closing. - EPSP |
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inhibitory
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- tranmsitter decreases the probability of AP firing (usually causes hyperpolarization)
- can involve K+ or Cl opening - IPSP: inhibitory post synaptic potential. |
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synaptic integration
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- neurons recieve multiple synaptic inputs
- neurons integrate (combine) the number, amplitude, rate of decay, and timing of EPSP's and IPSP's in deciding to fire action potentials. - temporal summation - a nuron adds the postsynaptic potentials arriving at its dendritic tree within a time interval. - spatial summation - a neuron adds the post synaptic potentials from multiple inputs throughout its dendritic tree. |
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fast vs. slow epsp's
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- an epsp mediated by ionotropic receptors (neuron 1) lasts fro milliseconds, while an EPSP mediated by metabotropic receptors can last for over a minute.
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axo axonic synapses
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- can enhance or inhibit transmitter release.
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convergence and divergence
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- convergence -
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NT classification of NT's
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- classical (small and rapid acting)
- aa and derivatives (glutamin, glycine and GABA) - AcH - monoamines - only one classical transmitter is released at the synapse. 2. Neuropeptides - large, slow acting - 3-100 aa's - often co released with classical transmitter - can be neuromodulators - modify action of classical NT's - endogenous opioids is an ex. 3. unconventional (unusual and controversial) - may not meet all the criteria for transmitters. |
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glutamate
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- the major excitatory NT in the brain and spinal cord
- ampa receptor/ channel - Na/ K channel; very fast EPSP's (fast signalling) - rolesare fast excitatory transmission, learning and memory. - NMDA receptors and channels - NA/Ca/K channel, used for slower, prolonged phase of EPSP. - information processing - Ca2+ entry - temporal summation - active only during strong stimuli. - Roles - cognition, learning and memory, motor control. - excitotoxicity - stroke, alzheimers disease, huntingtons disease - targe of abused drugs like alcohol, PCP (angel dust) - metabotropic glutamate recepots - 2nd messengers coupled - roles are cognition, learning and memory and motor control. |
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GABA
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1. the major inhibitory nt in the CNS
2. Gaba a R's - Cl- channel ; ver fast ipsp; postsynaptic - roles; fast inhibitory transmission, memory mood and motor control. - site of action of many drugs like anasthetics, sedatives 3. GABAb R's - coupled to K channel (opens) slow IPSP and PRESYNAPTIC - roles are slow inhibitory transmission, motor control, pain sensation and mood. GLycine - The major inhibitory transmitter in the spinal cord - glycine receptors - Cl channel is postsynaptic - roles are fast inhibitory transmission, motor control and sensation - stychnine poisoning |
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NE roles in CNS
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- sleep and wakefulness, attention and appetite.
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dopamine
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transmitter in the CNS
- 5 types of receptors (1-5) coupled to G proteins (modulate ion channels and 2nd messengers) - roles; motor control, motivation and reward (addiction) and mood. |
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serotonin
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- transmitter in the CNSwith many types of receptors most of which are coupled to G proteins.
- Roles are mood (depression and anxiety) motivation, sleep and wakefulness |
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acetylcholine
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- transmitter at the NM junction in CNS and its in the ANS.
- nicotinic receptors - Na k channels open - muscarinic receptors are coupled to G proteins which modulate ion channels and 2nd messengers - roles int eh CNS are learning and memory. |
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Neuropeptides
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Substance P - transmitter at pain pathways in the spinal cord
- enkephalins and endorphins - endogenous opioids; act in the brain and spinal cord - produce analgesia by inhibiting substance P. |
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Neuropeptides cont.
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- unconventional NT's
- NO, CO are gases - Cannabinoids - endogenous marijuana like compounds - backward (retrograde) transmission across synapse - modify presynaptic neuron actiity (inhibit NT release_ - imp. in appetite, learning and memory, cognition, judgement and mood. |
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cessation of Transmitter action
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- why is fast cessation of transmission needed - for cell to reset to its normal state
- better temporal resolution for fast processing. - enzymatic destruction - one or more enzymes break down the NT - e.g. acetylcholinesterase breaks down ach to choline and acetate very fast, thi is a target of insecticieds and nerve gases. - peptidases - nonspecifically degrade peptids more slowly and ACHE - reuptake - transporters remove released transmitter from the cleft EAAT (excitatory amino acid transporter) - transports glutamate into astrocytes using the Na gradient - Monoamine transporters (NET, DAT and SERT) Primary means of termination fo monoamine action. |
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cessation of transmitter action
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diffusion - peptides diffuse out of the cleft before nonspecific degradation.
- glutamate diffuses out of the cleft before reuptake. - can be very fast if the transmitter conc. is high. (mM) - desensitization (NT stays and receptor desensitizes) - receptors inactivate state despite bound transmitter - depends on receptor type; eg some ampa receptors have very fast desensitization. |
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pharmacological manipulation of synaptic function.
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- inhibition of NT release
- tetanus toxin - from bact. in wounds - inhibits release of GABA and glycine by preventing vesicle fusion. - decreased inhibition of motor neurons --> muscle contraction (tetanus) - botulinum toxin (botox) - inhibits release of AcH by preventing vesicle fusion - inhibition of motor neurons --> paralysis - Opioids - open a presynaptic K+ channels --> hyperpolarization - block substance P release |
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inhibition of NT uptake
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- antidepressents - Inhibit NET, SERT
- cocaine - inhibits DAT; dopamine builds up and causes CNS stimulation. |
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receptor antagonists
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- dopamine receptor antagonists - antipsychotics
- opioid receptor antagonists - heroin overdose; alcoholism - NMDA receptor antagonists - PCP - angel dust - ketamine- dissociative anasthetic used in children. Nicotinic AcH receptor antagonists - curare - blocks NM junction --> paralysis ; south american arrow poison. - Receptor agonists - opioid receptor agonists - morphine, oxycodone and heroin - receptor modulators - GABAa Receptors - valium (a benzodiazapene) - INcrease GABA affinity (binding) - antianxiety, sedative and can impair memory. |
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stimulus
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modality - kind of sensation (taste, touch, etc)
- affect - subjective perception of the stimulus, the feeling ass. with the stimulus(happy, sad, taste aversion - adequate stimulus - usual and appropriate stimulus for agiven receptor. receptors respnot best to one type of stimulus. - labeled line principle - sensory nerve just carries one type of info. although it may be able to sense more than one stimulus. |
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transduction principles
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- if a receptor only has a graded potential then it will not be felt; must be enough for an AP.
- for a long stimulus above threshold. - you fire a train of AP's - long stimulus with higher intensity; you get a higher frequency of AP's - limit on the frequency of firing AP's, but there is still a huge intensity range (IE hearing a whisper vs. an explosion) - also, a stronger stimuli could just lead to more receptors activated. |
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compression
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- a wide range of stimulus intensities encoded into a narrow range of responses
- Weber: Fechner priniciple - there is a logarithmic relationship between stimulus strength and response. |
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adaptation
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the way receptors detect stimuli over time
- tonic response - slowly adapting (a) IE - proprioception, sensing constant pressure. Used for things that are closely monitored. - phasic response - very rapidly adapting IE - Olfaction, sensing on and off pressure. |
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autism
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- inability to filter out unimportant stimuli
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accomodation
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- increase in the ap threshold
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acuity
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- sharpness, ability to distinguish the location of sensation
- receptive field - physical area that is covered by one sensory neuron - can vary in size and nubers - somatosensory cortex - differentparts of the body have different area sizes on the cortex. |
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lateral inhibition
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- inhibiting info. from neighboring sensory receptors. Lateral inhibition of weak stimulus happens in spinal cord by glycine release. glutamate is excitatory for the strong stimulus to continue to the brain.
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touch receptors
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- merkels discs - slowly adapting; sense steady pressure
- tactile discs - group of merkels disks - meisners corpuscles - rapidly adapting, sense changing pressure - pascinian corpuscles - both in deep layers of the skin and subcutaneous. they are very rapidly adapting, able to sens vibration and other rapid movement. - ruffini endings - tend to be in the deep skin layers. They sense stretch, heavy pressure and are slowly adapting. - hair gollicle receptors - nerve ending wrapped around a hair follicle. Slowly adapting, sensing touch or movement of the hair. |
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pain receptors
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- nociceptors - detect noxious stimuli. Free nerve endings sensing chemicals, temp. and mechanical stimuli causing tissue damage of the potential to. and they are slowly adapting.
- somatic pain - superficial - on body surface, mediated by myelinated A delta fibers - deep - inmuscles and joints, mediated by unmyelinated C fibers - visceral pain - mediated by slower C fibers - referred pain - like having a sore left am with heart attacks. Visceral pain reffered becauses they use the same sensory tracts as the overlying skin. |
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autonomic nervous system
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- general role - control of involuntary body functions
- endocrine - release of hormones into the blood - exocrine - secretion into GI tract - smooth muscles - GI tract, blood vessels, air flow - cardiac muscles for force of contraction etc. |
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sympathetic axon arrangement
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- short pre ganglionic axons and long post ganglionic axons. so ganglion is close to the spinal cord.
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parasympathetic axon arrangement
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- have long pre ganglionic axons and short post ganglionic axons so ganglion is close to effector organ.
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two neuron chain
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- ganglion - collection of CNS bodies outside the CNS
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axonal varicosities
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- specialized types of terminals, swellings along the length of an axon. Have NT vesicles.
- can innervate a broad area of effector tissue. - for when you don't need very specific control. |
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ANS innervation
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- some exceptions - blood vessels not innervated by PNS, only sympathetic
- decrease tone - vasodilation - increase tone - vasoconstriction - vagus is main parasympathetic outflow from CNS - sympathetic is very wids spread but can be very precise ; innervation of the eye. - one preganglionic neuron stimulates 100 postganglionc neurons( a wide convergence) |
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adrenal medulla
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- special part of SNS that is in teh endocrine system (inner part of the adrenal glands)
- releases epi and ne from chromafinn cells in post gang. neurons into the blood which act as hormones, which allows effects to last longer - modifiied sympathetic ganglion - collection of nerves outside the cns |
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chrmafin cells
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- modified secretory cells
- innervated by PRE ganglionic sympathetic axons. - release epinepherine (about 90% into the blood) - longer lasting effect, canreach organs not innervated by symp. fibers. - |
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selectivity of epi vs. NE
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- NE acts on alpha and Beta 1 R's
- epi acts on alpha, beta 1 and beta 2 R's since aireways have beta 2 R's on them epi causes dilation and helps breathing. |
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CNS pathology 2
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CNS infections
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CNS infections
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- meningitis - infection/ inflammation of the meninges in the subarachnoid space. wat to catch quickly because it can be fatal
- signs and symptoms - fever, headache, neck stiffness, mental confusion that comes on rapidly. - |
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genetic disorders of the CNS
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- neurofirbromatosis - (von reckinghausens disease) fairly common, with multiple types. Progressively disfiguring through life. tumore suppresor gene is inactivated. Genetic, but also can happen spontaneously
- neurofibromas - multiple rubbery painless nodular skin lesions. These are benign tumore of the peripheral nerves composed of schwann cells and fibroblasts. - gliomas - on the optic nerve - cafe aulait spots - skin lesions that are hyperpigmented. more than 6 are abnormal. - malignant potential - fibromas can be malignant fibrosarcomas. People with this can have in aincreaeed risk of getting other tumors. |
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facial pain etiology
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- TMD
- masticatory muscle disorders - dental and periodontal disease - neurological disorders |
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disorders that may mimic TMD
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- carotidynia - pain at ant. neck, continuous, throbbing and tender over carotid bifurcation.
- sinusitis - continuing aching and throbbing pain over temporal region, forehead, infraorbital region or in max. molar and premolar areas. - pulpitis |
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MS
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etiology - autoimmune disorder. antibodies from to the myelin and the myelin is destroyed. Cause is unknown, possible genetic component.
- pathologic features - MS plaques - areas of demyelination that occur through the cns. inflammation, and gliosis. - demyelination - hallmark of disease, of individual nerve fibers. leads to impaired function. also destruction of axons, which are severe. - signs and sx - varied and depend on cns region involved - sensory loss or parasthesia , weakness, fatigue, spasticity, visual deficits. - all lead to impaired and eventually blocked conduction. - pregression is variable and relapsing/ remitting form is most common. - 4 different types - gradually get worse. - gradually get better and then come back. and remyalination can occur. |
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alzheimers disease
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- pathologic features
- pregressive and irreversible lsos of neurons; esp. in cortex and hippocampus. - amyloid angiopathy - protein can be deposited in the walls of brain arteriolse, weakening them, leading ot small stroke events. - signs and symptoms - progressive impairments |
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parkinsons disease
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- 2nd most degenerative disease
- pathology features - loss of dopaminergic neurons; esp. in substantia nigra - lewy bodies - cytoplasmic protein deposits, thought to be toxic. - signs and symptoms - parkinsonism - caused by loss of dopamine neurons, resting tremor, slowness of movement, rigidity shuffing gait, flexed posture, difficulty in initiating movement, cognitive impairment, anxiety, depression, sleep disturbances and pain - clinical course - steady progression, may coexist with alz. boxers are predisposed to this sincey they have damaged da neurons. |
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ALS
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- etiology - unknown may be superoxidedismutase mutasted in people with the disease. usually involved in pretection from oxidation.
- pathologic features - loss upper and lower motor neurons - muscle atrophy secondary to the loss of innervation(lower motor neurons) - signs and symptoms - weakness of hands, cramping and spasticity in the arms and legs. clinical course - relentlessly progressive typically over 3-5 year, tends to strike people in middle age. death occurs from resp. paralysis. |
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diseases of the inner ear - often produce neurodefness/ neurological hearing loss
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- spreading infections from otitis media
- noise induced - hearing loss/ acoustic trauma - loss if iner ear hair cells. - can't regrow hairs - about 50% of people in the US with hearing loss caused by acoustic trauma. - decibels - 85 by a subway, prolonged, can cause a hearing loss 130 decibels; immediate damage - tinnitus - ringing out the ears. High pitched, usually idiopathic. doesn't cause hearing loss by itself. could be caused stress, taking a lot of aspirin. |
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meneire disease
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very rare, has an interesting triad of findings
- tinnitus - dizziness(vertigo) irreversible neurodefness - unknown etiology - tx - increase salt uptake - drug induced hearing loss - older antibiotics could damage the inner ear. - streptomycin and dihydromycin - aminoglycoside; main cause - acoustic neuroma - a benign brain tumor in the internal auditory meatus. - 8th CN - pretty rare |
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conjunctivitis
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- pink eye
- clinical findings - inflammation, pink, blood shot, hard to be inthe light - etiologies - viruses, bacteria, foreign bodies and allergies - keratitis defined - inflammation and scarring of the cornea (becomes opaque) , causes vision deficiency or blindness. main cause is herpes simplex virus 1. - swimmers eye - self limiting chlymidia, you get conjunctivitis but not keratitis. |
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trachoma
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- cause is bacterial
- chlamydia trachoma results in keratitis and scarring of cornea. big cause of blindness in 3rd world countries. |
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blepharitis - acute inflammation of eyelids.
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- these are small abscesses that involve eyelid margin.
- often biopsied because they look similar to eye cancer |
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sjogrens syndrome
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- dry eyes, keratoconjunctivitis, dry mouth and dry throat, a triad.
- autoimmune antibody antigen reaction in the lacrimal glands, leading to acute and chronic inflammation. producing a scar which shuts down th glands. - untreatable. - one serious complication; about 10% of these patients develop malignant lymphoma. |
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cataracts
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- involves the lens becomeing opaque to some degree.
- the usual causes are aging, uv radiation and diabetes. - tx - remoe the lens and put in a prosthetic. |
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retinal detachment
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- a seperation between the neurosensory retina and the retinal pigmented epithelium
- causes are often trauma to the eyes, malignant eye tumore and diabetes - may develop retinal infarction because the choroid coat supplies some of the blood supply to th pigmented retina. - should be treated by reattachment procedures. |
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hypertensive retinopathy
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- retinl path. caused by untreated history of hypertension.
- many dev. retinal hem. and ischemia. - diminishes number of blood vessels and calcification of blood essels. |
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diabetic retinopathy
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- may produce retinal hemorrhage and microaneurysms of the retina.
- surface of the moon look/ cotton wool appearance - blood vessels diminished, arterioles abnormally dilated leading to aneurysms. |
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glaucoma
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- normally , aqueous humor is produced by the ciliary bodies. this flows into the ant. chamber and exits by way of the canal of schlemm
- when glaucoma develops their is often an obstruction of some type preventing the aqueous humor from draining into the canal of schlemm. the ciliary bodies continue to produce humor .. this raises the intraocular pressure producing pressure necrosis of the retina. - if not treated necrosis of the retina may result in blindness. tx includes med. and topical meds to reduce the pressure. |
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macular degeneration
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- age related macular degeneration; macula degenerates and loses its cones. tend to get central visual field opaqueness.
- hard to treat since it is irreversible. |
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regulations of skeletal muscle activity
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structure of skeletal muscle
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- whole muscle is like bicep
- fasciculus - stringy part - muscle fiber - muscle cells, typically centimeters long with many nuclei, each innervated by one alpha motor neuron - myofibril - when you exercise you are increaseing the number and size of these. sarcomere - sections along the myofibril - myofilaments - make up sarcomere, the thick and thin filaments give skeletal muscle its striated appearance. |
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sarcomere structure
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- Z lines - distance between 2 z lines is a sarcomere. where the thin filament attaches
- the Z lines pull in towards each other during contraction - thick filament - inbetween the z lines - cross bridges - part of the thick filament where the thick and thin filaments attach. - H zone - region where there is only thick filament. - A band - length of the thick filament - only one that doesn't change length during contraction. - I band - where there is only thin filament. |
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myofilaments
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thick and thin
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thick filaments = myosin
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- light meromyosin end (tail)
- heavy meromyosin end is head has 2 regions (crossbridge) - S1 region = head - S2 region = forms a flexible leink between tail and head region. This is the region that moves during contraction. - heavy meromyosin head has 2 important binding sites. - actin binding site - where it binds to teh thin filament - atp binding site - an atpase that will break down atp for contraction. - two myosin molecules form a dimer, and many myosin dimers link together to form a chain which is the myofilament. |
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thin filament
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- made up of 3 different proteins.
- actin is the main component - G actin monomer; each one has a myosin binding site where the actin binds to the thick filament. - monomers form into long strings and 2 long strings come together to form the F actin filament. - F actin filament has helical structure. - under resting conditions, F actin cannot bind because of protein tropomyosin (lies in groove of the thin filament) - blocks the actin binding site. - troponin - has 3 binding sites - TnT - binds to tropomyosin - TnI binds to actin - TnC binds to calcium - when ca binds to troponin it causes tropomyosin to shift, exposing the myosin binding sites on actin, allowing contraction to occur. |
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sarcoplasmic reticulum
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- cell membrane called sarcolemma in muscle fibers
- transverse tubules - folds into the int. of the mscule cell in places - sarcoplasmic reticulum - inside cell, specialized ER that contains high levels of calcium. - innervation by alpha motor neuron which transfers AP to muscle cell which goes down the t tubule and causes contraction. |
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excitation - contraction coupling - how AP's cause contraction.
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- sr is reeally close to t tubule
- ryanadine receptor is a calcium channel in SR - dihydropyridine - in wall of t tubule - blocks ryanadine receptor channel. - ap travels down the t tuble and causes the dhp rec. to remove from the ryanadine receptor which allows ca to be released.. this causes myofilament contraction and will contract as long as calcium is out there and it is pumped back into the sr by a calcium pump that uses ATP |
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contraction
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occurs when myosin binding site and actin binding site come together
- blocked by tropomyosin - troponin causes tropomyosin to move out of the way for contraction. |
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cross bridge cycle
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- 1. resting state - actin and myosin not bound, myosin in a high energy state
2. add ca to myoplasm (a+ myosin+ adp + pi) actin and myosin bind together - then adp and pi fall off of myosin - powerstroke occurs; crossbrideg bends, actin shifting along myosin(the movement) energy comes from myosin in its high energy stae 3. actin and myosin are together and myosin is in a low energy state. 4. ATP binds to myosin, which causes the actin and myosin to split apart - ATP binds to myosin on the S1 region of the head. 5. atp undergoes hydrolysis --adp and pi - this energy puts myosin back into a high energy state 6. to turn off powerstroke pumpca back into sr |
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skeletal muscle mechanics
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control of strength of contraction
- motor unit recruitment - send ap's down multiple motor units. - summation and tetany - high frequency of aps down each alpha motor unit. - twitch contraction - ap off by itself on the graph - summation - when the AP are coming too fast for the cell to go back to normal levels before the next one comes. of the contraction, not the ap. 3. tetany - muscle always contracted. Muscle begins to fatigue. use dependent decrease inforce. - fatigue - not due to decreased levels of ATP More likely due to increased H+ and pi which inhibit ca binding to troponin. 4. for both ca builds up in the myoplasm. |
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muscle fiber length - not as critical in skeletal muscle as cardiac.
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- muscle too short; not enough force, crossbridge cannot form properly due to overlap of thin filaments.
- maximum shortening: the length of the thick filament. 2. optimum length - high levels of force, crossbridges can form properly 3. too long/ stretched - only low levelsof force crossbridge doesn't form properly. |
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types of contraction
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isometric
isotonic |
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isometric contraction
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- where muscle is prevented from shortening (length does not change) but you generate force (atp is used)
- used to measure ability to generate force |
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isotonic contraction
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- to get to an isotonic contraction you have to first have an isometric contraction (to generate enough force to overcome the weight of the object)
- used to measure shortening velocity. |
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skeletal muscle energetics
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- atp production and use
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creatine phosphate
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- when it goes from creatinephosphate to creatine you take adp --> atp.
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oxygen debt
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- increased oxygen consumption following exercise
- as you exercise you ahve a lack of oxygen to the muscle so you have increased glycolysis and increased lactic acid buildup. - when you stop exercising, you need additional oxygen to send lactic acid through krebs cycle. |
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smooth muscle mech. of contraction
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- role of ca - increased ca in the myoplasm causes contraction.
- regulates THICK filaments (skeletal is thin) - ca comes from teh SR and from outside the cell so 2 instead of 1 source. - ca acts on calmodulin and myosin light chain kinases. when resting these do not interact with eachother. - 4 Ca will bind to CaM, which causes it to interact with MLCK - CaM activates MLCK - MLCK phosphorylates mysoin and thus myosion is activated - when myosin is activated, it goes through crossbridge cycling - crossbridge cycling will continue for as long as myosin is phosphorylated. - atp doesn't break apart the myosin and actin. - myosin light chain phosphatase dephosphorylates the myosin, deactivating it and stopping the crossbridge cycling. - thus, contraction is controlled by the cons. of MLCK vs. MLCP - MLCP is always active - MLCK is what is regulated (dominant in high levels of ca and contraction occurs) - to get rid of ca you actively transport the ca out of cell or bakc into sr. |
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latch state
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- maintain contraction with little atp use
- to get into latch state, you need some increase in myoplasmic ca levels. but not high enough to cause crossbridge cycling. - crossbridge cycling is very slow, so that the actin and myosin remain attached. |
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control of motor activity (electrical activity)
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- change in membrane is due to pacemaker cells (intrinsic property of teh cell)
- force of contraction will follow the activity of the pacemaker cells - on depolarization it opens voltage gated ca channels letting ca into the cell and causeing contraction. - in sm. mus. there is always tone - nervous system activity shifts the polarization to depolarization which causes greater forces of contraction, OR hyperpolarization which decreases force of contraction. |
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source of ca
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increasing contraction
- regulated by NT binding to a receptor opening a sodium channel which would increase the amount of Ca coming in and more contraction - NT binding to K channel which would hyperpolarize the cell and thus decreease the amount of contraction adn calcium - NT can activate a second messenger pathway, producing IP3, IP3 acts on SR to cause the release of CA increasing the amount of Contraction. - ca induced ca release - calcium coming into cell from the outside stimulates the SR to release more calcium - stoppintg contraction occurs by pumping ca out of the cell or back into SR via active transport. |
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lenth tension relationship
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- sm. muscle works over a larger range of length because it doesn't have sarcomeres.
- max. force is the same for both types (just takes sm. muscle longer to generate it) |
