2 Neuroscience2.4 Cells

2.4.2 Fundamental physiology of neurones, synapses and receptors

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Written by Resident Doctor Committee · Published

Resting membrane potential

  • The resting membrane potential of a typical neurone is about -70 mV, inside negative.

  • Potassium is the most concentrated ion inside the neurone at rest, including in the axon terminal, while sodium is concentrated outside.

  • The sodium-potassium ATPase holds these gradients, pumping three sodium ions out for every two potassium ions in.

  • The resting potential is set chiefly by potassium leaking out through channels open at rest.

Ion

Movement across the resting membrane

Chloride

Crosses freely and distributes passively, close to electrochemical equilibrium (about -70 mV in adults)

Potassium

Crosses relatively readily

Sodium

Hardly crosses, so is largely excluded at rest

Large organic anions

Hardly cross

The action potential

  • Threshold is about -55 mV, roughly 15 mV above rest: there, opening of voltage-gated sodium channels becomes self-sustaining and the neurone fires.

Phase

What happens

Rising

Voltage-gated sodium channels open and sodium flows in; each opening depolarises the membrane further, towards the sodium equilibrium potential (+60 mV), peaking at +30 to +40 mV

Peak

Sodium channels inactivate and potassium conductance rises

Repolarisation

Voltage-gated potassium channels open a fraction of a millisecond after the sodium channels, and potassium flows out

After-hyperpolarisation (undershoot)

Potassium channels close slowly, so efflux persists and pulls the membrane towards the potassium equilibrium potential, near -90 mV

In panel A, follow the trace from rest at about -70 mV through threshold at about -55 mV to a peak near +40 mV, then down through repolarisation into the after-hyperpolarisation undershoot below the resting potential. Artwork by Synaptidude at en.wikipedia, CC BY-SA 3.0, via Wikimedia Commons
  • Spikes are all or none, so stronger input changes their rate or timing, not their amplitude.

Refractory periods and conduction

Period

Cause

Response

Absolute

Voltage-gated sodium channels are inactivated and cannot reopen until the membrane repolarises

No stimulus can trigger a spike

Relative

Sodium channels have partly recovered and potassium conductance stays raised

A stronger stimulus is needed

  • Myelin raises membrane resistance and lowers capacitance, so spikes regenerate only at the nodes (saltatory conduction); demyelination slows or blocks conduction.

Synapses

  • At a chemical synapse, the presynaptic spike opens calcium channels, and calcium triggers vesicle fusion and transmitter release.

  • Uptake, metabolism and diffusion clear the transmitter.

  • Electrical synapses are gap junctions, formed by paired connexons, that pass current rapidly in both directions.

  • They are abundant in the retina, for example between horizontal cells, and in the cerebral cortex, where they can synchronise interneurones.

The link from photoreceptor to bipolar cell is chemical, not electrical.

Receptors

  • Ionotropic receptors are ligand-gated channels with rapid effects, whereas metabotropic receptors, often seven-transmembrane G protein-coupled receptors, act through intracellular signalling with slower, longer-lasting effects.

  • Allosteric modulators bind away from the transmitter (orthosteric) site; benzodiazepines, for example, enhance the response at gamma-aminobutyric acid type A (GABA-A) receptors.

  • Autoreceptors respond to the cell's own transmitter and heteroreceptors to another, and both regulate release.