C2.2 Neural signalling

When you snatch your hand from something hot, electrical and chemical signals race through your nervous system in a fraction of a second. Neural signalling is how neurons carry information rapidly over long distances and pass it from cell to cell. For C2.2 the story has two halves: how an action potential travels along a single neuron as an electrical signal, and how it crosses the gap between neurons at a synapse as a chemical signal. Keep that electrical-then-chemical structure in mind and the detail falls into place.

Neurons and the resting potential

A neuron is specialised to carry electrical impulses. Dendrites and a cell body receive signals, a long axon carries the impulse, and many axons are wrapped in a fatty myelin sheath that speeds transmission. Before any signal travels, a resting neuron maintains a resting potential — a voltage of about −70 mV across the membrane, with the inside negative relative to the outside.

This difference is set up by the sodium–potassium pump, which uses ATP to move three Na⁺ out of the cell for every two K⁺ pumped in. Together with the membrane’s differing permeability to these ions, this creates an uneven distribution of charge: the membrane is polarised. The resting potential is the charged-up state the neuron holds, ready to fire.

The action potential

An action potential is a rapid, temporary reversal of the membrane potential. If a stimulus depolarises the membrane past a threshold, voltage-gated channels open and the signal fires fully — the all-or-nothing principle: a stronger stimulus does not make a bigger impulse, only more frequent ones.

• Depolarisation: voltage-gated sodium channels open, Na⁺ rushes in, and the inside becomes positive (up to about +30 mV).
• Repolarisation: sodium channels close and voltage-gated potassium channels open, so K⁺ leaves and the inside becomes negative again.
• Refractory period: the membrane briefly cannot fire again, which ensures the impulse travels in one direction only.

The sodium–potassium pump then restores the original ion distribution. The action potential is regenerated along the axon, so it does not weaken with distance.

Propagation and the role of myelin

An action potential at one point depolarises the next stretch of membrane, triggering a new action potential there, and so the impulse moves as a self-renewing wave. In myelinated neurons the sheath insulates most of the axon, leaving small gaps called nodes of Ranvier. The action potential effectively jumps from node to node — saltatory conduction — which makes transmission much faster than in unmyelinated axons.

Speed therefore depends on myelination and on axon diameter (wider axons conduct faster). This is why reflexes that protect the body, served by myelinated neurons, are so rapid. A common exam point: myelin saves energy as well as time, because depolarisation only happens at the nodes.

Synaptic transmission

Neurons do not touch; they are separated by a tiny gap, the synaptic cleft. Because the electrical impulse cannot jump this gap, the signal is passed chemically. When an action potential reaches the end of the presynaptic neuron, it triggers the following sequence:

• Voltage-gated calcium channels open and Ca²⁺ enters the presynaptic terminal.
• This causes vesicles of neurotransmitter to fuse with the membrane and release their contents by exocytosis.
• The neurotransmitter diffuses across the cleft and binds to receptors on the postsynaptic membrane.
• Binding opens ion channels, and if the postsynaptic membrane depolarises past threshold a new action potential is triggered.

The neurotransmitter is then rapidly removed or broken down (for example, acetylcholine is broken down by an enzyme), so the signal is brief and controlled. Because receptors are only on the postsynaptic side, the synapse also ensures the impulse passes in one direction only.