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Nerve AP & reflexes

The neuronal action potential and why it differs from the cardiac one, then monosynaptic versus polysynaptic reflexes and what happens to them in spinal cord injury.

The neuronal action potential

Resting membrane potential −70 mV, threshold −55 mV, peak +30 mV. Total duration only about 1–2 ms — a fraction of the cardiac action potential.

1

Depolarisation to threshold

A stimulus depolarises the membrane. At −55 mV the fast voltage-gated Na⁺ channels open and Na⁺ floods in.
2

Rapid depolarisation — the spike

Regenerative Na⁺ entry drives the membrane to about +30 mV. All-or-none: once threshold is reached the amplitude is fixed.
3

Repolarisation

Na⁺ channels inactivate and voltage-gated K⁺ channels open, so K⁺ efflux restores the negative interior.
4

Hyperpolarisation (undershoot)

K⁺ channels are slow to close, so efflux continues past the resting potential. This period underlies the relative refractory period.
5

Return to resting potential

The Na⁺/K⁺ ATPase (3 Na⁺ out, 2 K⁺ in) restores the ionic gradients. RMP is set mainly by K⁺ permeability, keeping the inside more negative.

The key contrast with cardiac muscle

The neuronal action potential has no plateau phase, so it lasts 1–2 ms rather than 200–300 ms.
Its refractory period is therefore very short — which is precisely why neurones CAN be tetanised and cardiac muscle cannot.
Skeletal muscle inherits this: rapid repeated stimulation produces summation and tetanic contraction.

Monosynaptic vs polysynaptic reflexes

	Monosynaptic	Polysynaptic
Synapses	One	Two or more
Interneurone	Absent	Present
Speed	Very fast	Slower
Reflex arc	Sensory → motor neurone	Sensory → interneurone → motor
Complexity	Simple	Complex
Function	Maintains muscle tone and posture	Protective and co-ordinated
Examples	Stretch reflex — knee jerk, ankle jerk	Withdrawal (flexor) reflex, crossed extensor reflex — e.g. touching something hot

The stretch reflex, step by step

Tapping the patellar tendon stretches the quadriceps.
The muscle spindle detects the stretch and fires impulses along Ia afferents to the spinal cord.
The sensory neurone synapses directly on the α-motor neurone — releasing glutamate, producing an EPSP.
The quadriceps contracts and the leg extends.
Simultaneously an inhibitory interneurone releases glycine onto the antagonist's motor neurone — an IPSP — relaxing the hamstrings. This is reciprocal inhibition.

Three facts worth having ready

All autonomic reflexes are polysynaptic, as are all nociceptive (pain) withdrawal reflexes.
The ankle jerk is initiated by stretch of the gastrocnemius (S1–S2). The knee jerk is L3–L4.
Glutamate is the main excitatory transmitter (EPSP); glycine is the main inhibitory transmitter in the spinal cord, GABA in the brain (IPSP).

Spinal shock — the sequence

Immediately after cord transection, all reflexes below the lesion are lost — flaccid areflexia, loss of tone, and loss of autonomic reflexes.
Eventually reflexes return and become exaggerated — hyper-reflexia, spasticity, clonus and an upgoing plantar, because descending inhibition has been removed.
Polysynaptic reflexes also become exaggerated. The transition typically takes days to weeks.
Practical relevance: this is the same denervation process that makes suxamethonium dangerous after about 24–48 hours in spinal cord injury, through extrajunctional receptor proliferation.

Built from handwritten pages IMG_0980, IMG_0981 and IMG_0990 (your page cites Dr Podcast p.72).