Nerve Physiology
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Direct answer
A large myelinated nerve fibre at rest holds its inside about 70 millivolts negative — the resting membrane potential, dominated by potassium leak channels — and when depolarisation crosses roughly 15-30 millivolts to threshold, voltage-gated sodium channels open and the all-or-none action potential overshoots to about +35 mV before delayed potassium efflux repolarises it. In myelinated fibres the impulse jumps node to node (saltatory conduction), reaching 70-120 m/s in A-alpha fibres while unmyelinated C pain fibres conduct below 2 m/s. Local anaesthetics block the sodium channel from the inner side; demyelinating disease slows or blocks conduction, the physiology beneath every Guillain-Barre and multiple sclerosis stem.
What you must remember
- Values to quote: resting potential about −70 mV in nerve (−90 mV in skeletal muscle); potassium equilibrium potential near −94 mV and sodium near +61 mV by the Nernst equation; the Goldman-Hodgkin-Katz equation blends them.
- Phases: depolarisation by sodium entry, repolarisation by potassium exit, then after-hyperpolarisation; the whole nerve spike lasts about 1-2 milliseconds.
- Absolute refractory period (sodium inactivation gates shut) caps firing frequency and explains unidirectional propagation; the relative refractory period needs a stronger stimulus.
- Fibre classification: A-alpha 70-120 m/s (motor, proprioception), A-beta touch, A-gamma motor to intrafusal fibres, A-delta fast pain, B preganglionic autonomic, C unmyelinated slow pain below 2 m/s.
- Nerve conduction study logic: demyelination slows velocity and prolongs distal latency; axonal neuropathy drops amplitude while velocity is relatively preserved.
- Seddon's injuries: neurapraxia (conduction block, early recovery), axonotmesis (axon severed, sheath intact, wallerian degeneration distally, regeneration near 1 mm per day), neurotmesis (whole nerve divided, needs surgery).
- Viva drugs: tetrodotoxin and local anaesthetics block sodium channels; ouabain blocks the pump; tetanus and botulinum toxins act on transmitter release instead.
Tracing an impulse down a motor axon
Begin at the soma, where thousands of excitatory and inhibitory postsynaptic potentials summate; the axon hillock, with the lowest threshold density of sodium channels, is where the decision to fire is made. Once initiated, the spike regenerates itself at each node of Ranvier: local current flows under the insulating myelin to the next node, depolarising it past threshold, so the impulse leaps forward without fading — myelin works by raising membrane resistance and lowering capacitance. At the terminal, depolarisation opens calcium channels, calcium entry fuses acetylcholine vesicles, and the quantal content of the end-plate potential crosses threshold in muscle — which is where the muscle physiology chapter picks the story up.
Now watch the same system fail, because examiners set disease on physiology. A man develops ascending weakness two weeks after a diarrhoeal illness: Campylobacter infection has triggered antibodies against myelin, conduction velocity falls sharply with prolonged distal latencies and conduction block on nerve conduction studies, and the CSF shows albuminocytological dissociation — Guillain-Barre syndrome, a physiology diagnosis before it is a clinical one. Contrast the pressure palsy from leaning on a nerve: conduction block without structural interruption, recovering in days to weeks — neurapraxia. And the crushed limb where the axon dies back: wallerian degeneration of the distal stump with chromatolysis of the cell body, regeneration crawling at about a millimetre a day, roughly an inch a month.
High-yield viva angles
Be ready to reason, not recite. Why does myelin speed conduction but also save energy? Because only nodal membrane depolarises, far fewer ions shift, and the pump does less restoration per metre travelled. Why does the action potential never decrement? Each node regenerates a full spike rather than passing a passive, fading current. Which fibres die first in hypoxia and which block first with lignocaine? Small unmyelinated C and small myelinated B fibres surrender before large A fibres, which is why a spinal anaesthetic takes away pain and autonomic tone before motor power. Expect one question on why the nerve cannot be tetanised at ordinary stimulus rates — the absolute refractory period enforces a ceiling on frequency.
Frequently asked questions
What is the ionic basis of the resting membrane potential?
Mostly potassium leak permeability pushing the membrane towards the potassium equilibrium potential near −94 mV, offset by slight sodium leak to about −70 mV, with the Na-K pump maintaining the gradients.
Why is conduction faster in myelinated fibres?
Myelin raises membrane resistance and lowers capacitance, so current jumps between nodes of Ranvier — saltatory conduction reaching up to 120 m/s in A-alpha fibres.
Which fibres carry pain, and which block first with local anaesthetics?
Fast sharp pain travels in A-delta and slow burning pain in C fibres; local anaesthetics block autonomic B and unmyelinated C fibres before large motor A fibres.
How do neurapraxia and axonotmesis differ?
Neurapraxia is conduction block without structural break, recovering in days to weeks; axonotmesis interrupts the axon with wallerian degeneration but keeps the connective sheath, so regeneration proceeds at about 1 mm daily.
What does nerve conduction testing show in Guillain-Barre syndrome?
Demyelination slows conduction velocity, prolongs distal latencies and produces conduction block, with relatively preserved amplitudes in the early demyelinating pattern.