Physiology · Short notes

Neurophysiology: Short Notes & Cheat Sheet

Resting and action potentials, nerve fibre types, synaptic transmission and neurotransmitters, reflexes, motor lesions and sleep.

Short notes

Read these before you attempt the topic's MCQs.

An action potential, step by step

1Resting≈ −70 mV2Threshold≈ −55 mV3DepolarisationNa⁺ rushes in4Peak≈ +30 mV5RepolarisationK⁺ moves out6HyperpolarisationBrief overshoot, then rest
Sodium channels open first and fast; potassium channels open later and close slowly, causing the brief overshoot.

Membrane potentials

  • Resting membrane potential in neurons is about −70 mV, set mainly by potassium leak and maintained by the Na⁺/K⁺-ATPase (3 Na⁺ out, 2 K⁺ in).
  • At threshold (about −55 mV) voltage-gated sodium channels open and sodium rushes in (depolarisation, peaking near +30 mV).
  • Potassium then leaves (repolarisation), briefly overshooting (hyperpolarisation).
  • Action potentials are all-or-none. The absolute refractory period stops a new impulse; the relative one needs a stronger stimulus.
  • Myelinated fibres conduct faster by saltatory conduction between nodes of Ranvier.

Fibres and synapses

  • Aα fibres are the largest and fastest (motor, proprioception). C fibres are small, unmyelinated and slow (dull pain, temperature, postganglionic autonomic).
  • Local anaesthetics block small fibres first, so pain goes before touch and movement.
  • At a synapse, calcium entry releases neurotransmitter, which produces excitatory or inhibitory postsynaptic potentials that summate in time and space.
  • Main excitatory transmitter in the brain: glutamate. Main inhibitory: GABA in the brain and glycine in the spinal cord (strychnine blocks glycine receptors).
  • At the neuromuscular junction, acetylcholine acts on nicotinic receptors to produce the end-plate potential.

Reflexes, lesions and sleep

  • A reflex arc has a receptor, afferent nerve, integrating centre, efferent nerve and effector. The knee jerk (L3–L4) is monosynaptic.
  • Upper motor neurone lesions cause spasticity, brisk reflexes and an upgoing plantar (Babinski sign).
  • Lower motor neurone lesions cause flaccid weakness, wasting, fasciculation and reduced reflexes.
  • The corticospinal (pyramidal) tract crosses in the medulla; pain and temperature travel in the spinothalamic tract.
  • EEG waves: beta (alert), alpha (relaxed with eyes closed), theta (drowsy) and delta (deep sleep). REM sleep is when most dreaming occurs.

Cheat sheet

High-yield facts in one place. Cover the right-hand column and test yourself.

Neurotransmitters

TransmitterMain role
GlutamateMain excitatory (brain)
GABAMain inhibitory (brain)
GlycineInhibitory (spinal cord)
AcetylcholineNMJ, autonomic, memory
DopamineMovement, reward, prolactin inhibition
SerotoninMood, sleep, nausea
Substance PPain transmission

UMN vs LMN lesion

SignUMN · LMN
ToneIncreased (spastic) · decreased (flaccid)
ReflexesBrisk · reduced or absent
WastingLittle · marked
FasciculationNo · yes
Plantar responseUpgoing (Babinski) · downgoing

Memory aids

Sodium Swings up, Potassium Pulls down
Na⁺ influx depolarises; K⁺ efflux repolarises.

Exam traps

  • The resting potential depends mainly on potassium, not sodium.
  • Glycine, not GABA, is the main inhibitory transmitter in the spinal cord.
  • An upgoing plantar response indicates an upper motor neurone lesion.
  • Unmyelinated C fibres conduct slowest; they carry dull, burning pain.

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