Nerve and Muscle Physiology
- Created by: rosieevie
- Created on: 19-01-17 12:34
Divisions of the Nervous System
CNS:
- Brain
- Spinal Chord
PNS:
- Sensory divison - detects environmental changes
- Motor division
- Somatic - voluntary
- Autonomic - involuntary
- Sympathetic - increases to norm
- Parasympathetic - decreases to norm
Spinal Cord and PNS
Grey matter - cell neuron bodies
White matter - fibre tracks (milanated axons)
Dorsal root ganglion - cluster of nerve cell bodies outside CNS
Dorsal root - where afferent fibres enter spinal chord
Ventral root - where efferent fibres leave spinal chord
Afferent fibre - carry signals to CNS (sensory info)
Efferent fibre - carry signals from CNS to PNS (motor info)
Nucleus - nerve cell body cluster within CNS
Reflex - predictable stereotypical response to specific stimulus
Renshaw cells - inhibatory cells stopping other neurones becoming excited (lateral inhibiton)
Monosynaptic Neural Simple Reflex Circuit
- Extensor muscle stretched and muscle spindle stimulated
- Primary afferent neuron excited
- Synapse
- Efferent alpha motor neuron stimulated
- Extensor muscle stimulated and contracts
- Flexor muscle relaxes
1 synapse, 2 neurones
Autonomic Motor Division - Involuntary
- Sympathetic - stress
- Parasympathetic - resting conditions
Sympathetic and Parasympathetic Nervous System
- Effect always have at least 1 synapse in outside CNS ganglion
- Preganglionic efferent axons myelinated
- Chloinergic ganglionic synapses - acetylcholine
- Postganglionic non-myelinated
- Postganglioninc neurones form plexi (spinkler system) w/ many synapses
Neurone
- Dendrite - branches recieving signals, contain postsynaptic membrane
- Soma - cell body containing nucleus and organelles
- Axon - output process, different extensions depending on neurone
- Boutons - swellings at axon terminals contain pre-synaptic memebrane
- Myelin Sheath - insulating layer to quickly conduct impulses (Schwann cells - glial)
- Nodes of Ranvier - gaps where action potential occurs
Exciting a Neurone
Resting membrane potential - high energy state
Outside = 0mV
Inside = -60mV (negative)
- More Na+ outside
- More K+ inside - leak out of cell (selective permeability to K+ ions)
- More Cl- inside
= CONCENTRATION GRADIENT (maintained by ion pumps against gradient e.g. Na+/K+ ATPase)
Electrogenic ion pump - pump unequal number of ions (3Na+,2K+) generates a electrical gradient
Increase concentration gradient -> K+ ions move down out fo cells = more -ve
Electrochemical Gradients
Electrochemical gradient - how far equillibrium potential is from resting membrane potential
Ions move down electrochemical gradient
Equilibrium - electrical gradient balances concentration gradient
Equilibrium potential (mV) - potential difference between 2 membrane sides
EmV = 61.5 log([K+out]/[K+in]) NERNST EQUATION
When the membrane = Emv there is no net flux of ions
Hodgkin and Huxley
Squid axon tested to see if EmV determined soley by K+ permeability
Should be straight correlation if just K+ ions
However - devaiation
MEMBRANE AT REST IS SLIGHTLY PERMEABLE TO Na+ - set by tansmembrane ion channels
Em = -60mv to -70mv
Goldman Constant Field Equation
60 should be 61.15
Ions
ECl<Em (more negative) due to ion exchangers -> increased Cl- hyperpolarises neurones
At rest Na+ ins not at equilibrium = high energy state
Stimulations
Weak Electrical Stimulaton
Electrotonic conduction - stimulus passively decreases in amplitde
Strong Electrical Stimulation
Generates action potential - propogates along axon
All or nothing response = axon havs threshold for activation
Action Potential
Measured using voltage-clamp technique.
Action potential spike due to transient increase in Na+ permeability (voltage-gated Na+ channels open) due to membrane depolarisation
Action Potential Explained
- Resting potential - PK>>PNa
- Passive depolarisation - no change in ionic permeability PK>>PNa
- Threshold potential - voltage-gated Na+ channels activated, Na+ current depolarises membrane PNa>>PK -> Em gets closer to ENa
- Postive feedaback cycle - more Na+ channels open
- Em overshoots 0
- Em approaches ENa (~+60mV) = current driving force decreases
- Na+ channels inactivate - time-dependent inactivation gate
- Delayed recifer K+ channels open, PNa decreases + PK increases re/hyperpolarisation
- Em returns to resting value but undershoots
- Both leaked and delayed K+ channels open - PK>>PNa = refractory period
- Both Na+ channels and delayed rectifier channels deactivate - Em returns resting value
Refractory periods
Absolute refractory period - inexcitable membrane as all Na+ channels inactivated
Refractory period - activation threshold is increase as some Na+ channels at resting state
Action Potentials are very Efficient
After adding a neurotoxin to nerve axon action potentials still conducted for considerable period of time after
Only a few ions are moved to generate action potentials as membrane is a capacitor - seperates and stores electical charge (around 1x10-12mol Na+ needed)
COMPOUND ACTION POTENTIAL - the sum of the action potentials in a bundle of axons
Compound action potential amplitude = how many axons excited and strength of stimulus
- Increases as stimulus increase until all axons in nerve are excited/recruited
Myelinated Neurones
Increases conduction velocity - increases out resistence:in resistence
- Peripheral nerves - Schwann cells
- CNS - oligodendrocytes
Unmyelinated axons:
- Adjacent regions exchange charge - depolarises next section
- Unidirectional
- Velocity ~5m/sec
- Increasing axon diameter increases velocity
Myelinated axons:
- Salatory conduction - AP skips between nodes of Ranvier
- Uniderctional
- Zero sigbal loss
- Small axon diameters
- Rapid transmission ~100m/sec
- Voltage-gated channgels at nodes of Ranvier
Ca2+ Dependence of Synapses
Ca2+ dependence of synaptic transmission
Possible to block Na+ chanels and record postsynaptic response = Na+ isn't cause
Removing extracellular Ca2+ abolished nerurotransmitter release.
Synapses
- Neurotransmitter synthesised and stored in vesicles
- Action potential at presynaptic bouton = depolarisation
- Voltage-gated Ca2+ channels open = Ca2+ into presynaptic bouton
- Vesicles fuse with presynaptic membrane
- Neurotransmitter released into synaptic cleft by exocytosis
- Neurotransmitter binds to receptor molecules
- Postsynaptic channels open/close
- Postsynaptic current causes excitatory or inhibitory potential that changes cell excitability
- Neurotransmitter deactivated by reuptake or enzymatic degredation
Excitatory/Inhibitory Postsynaptic Currents/Potent
Excitatory
Current dspolarizes postsynaptic membrane = potentials summate until threshold reached for action potential generation
Inhibatory Currents
Current flow through inhibatory neurotransmitter activated channels
Inhibatory Potentials
Summate to reduce excitability (hyperpolarise cells), reduce probability of action potential generation
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