Neural signalling transmits information through neuron structure, ion gradients, action potentials, synapses and chemical modulation of postsynaptic responses, linking cellular mechanisms to rapid communication in nervous systems.
| Neuron | Information route | Decisive structural pattern |
|---|---|---|
| sensory | receptor → CNS | long dendron toward an off-centre cell body; axon continues into CNS |
| relay | within CNS | many short dendrites and a short axon connect neurons locally |
| motor | CNS → muscle or gland | many dendrites around the cell body; one long axon reaches an effector |
Dendrites and dendrons carry impulses toward the cell body; an axon carries impulses away from it. A nerve is a bundle of many nerve fibres, not one neuron.
At rest, an axon's inside is about −70 mV relative to the outside. The membrane is polarized because ions and large negative solutes are distributed unequally across it.
The sodium–potassium pump hydrolyses ATP to move 3 Na⁺ out for every 2 K⁺ in, against both concentration gradients. It establishes and maintains high Na⁺ outside and high K⁺ inside.
At rest the membrane is much more permeable to K⁺ than to Na⁺. K⁺ leakage leaves behind impermeant negative charge, so the inside becomes negative. The pump maintains the gradients that this leakage continually uses.
An action potential is a brief reversal of membrane potential, typically from about −70 mV to about +40 mV. A nerve impulse is this action potential repeatedly regenerated along a nerve fibre.
Ion flow through open channels is passive, down electrochemical gradients. ATP is used by pumps to maintain and restore those gradients, not to push each ion through an open channel.
Transmission is normally one-way because release machinery is presynaptic while matching receptors are postsynaptic. Synapses can connect neuron to neuron, neuron to muscle, or neuron to a gland cell.
neurotransmitter diffuses across the cleft → binds a complementary postsynaptic receptor → ligand-gated cation channels open → Na⁺ entry depolarizes the membrane → an excitatory postsynaptic potential (EPSP) forms
An EPSP is graded: more transmitter can produce a larger local depolarization. It makes an action potential more likely, but only a summed depolarization reaching threshold triggers the all-or-none spike.
The signal must be removed. At cholinergic synapses, acetylcholinesterase hydrolyses acetylcholine; receptors close, and choline can be taken up for reuse. Other transmitters may be removed by reuptake or diffusion.
| Trace phase | Main channel event | Ion movement and voltage change |
|---|---|---|
| threshold and rising phase | voltage-gated Na⁺ channels open rapidly | Na⁺ enters; positive feedback causes steep depolarization |
| peak | Na⁺ channels inactivate; delayed K⁺ channels are open | inward current falls and outward K⁺ current dominates |
| falling phase | voltage-gated K⁺ channels remain open | K⁺ leaves; membrane repolarizes |
| undershoot | K⁺ channels close slowly | continued K⁺ exit briefly hyperpolarizes the membrane |
The Na⁺/K⁺ pump maintains the long-term gradients, but it does not cause the rapid falling phase. Repolarization is mainly produced by K⁺ leaving through voltage-gated channels.
Na⁺ entry makes one axon region positive inside. Positive charge spreads through the axoplasm toward the adjacent negative region, while return current flows outside the axon. This local current depolarizes the next membrane region.
If the adjacent region reaches threshold, its voltage-gated Na⁺ channels open and a new full-sized action potential forms. The signal is regenerated rather than a single electrical pulse fading with distance.
Saltatory conduction is faster and more energy-efficient than regenerating an action potential at every adjacent patch of membrane, because far less membrane exchanges ions.
An exogenous chemical originates outside the body. At a synapse it can mimic a transmitter, block a receptor, change release, prevent breakdown, or block reuptake.
| Chemical | Molecular target | Immediate synaptic effect |
|---|---|---|
| neonicotinoid | insect nicotinic acetylcholine receptor | binds persistently and disrupts cholinergic transmission; acetylcholinesterase cannot remove it |
| cocaine | dopamine reuptake transporter | dopamine remains in the cleft longer, so postsynaptic signalling is prolonged and amplified |
The same behavioural label—‘stimulant’—does not identify a molecular mechanism. Predict the effect by locating the chemical's target in the release–receptor–removal cycle.
| Summation | Inputs being combined |
|---|---|
| temporal | repeated postsynaptic potentials arriving close together from the same synapse |
| spatial | postsynaptic potentials arriving at about the same time from different synapses |
The axon initial segment integrates EPSPs and IPSPs across space and time. If net depolarization reaches threshold, a full action potential begins; if inhibition or decay keeps it below threshold, no action potential occurs.
Summation combines graded potentials. Action potentials themselves do not add into a larger spike.
noxious heat, cold, acid, chemicals or tissue damage → matching TRP or other sensory ion channel opens in a free nerve ending → positive ions enter → receptor potential reaches threshold → action potentials travel through sensory pathways → brain activity produces pain perception
TRPV1 responds to damaging heat and capsaicin; TRPA1 responds to several intense cold, reactive and damage-associated signals. Inflammation can lower activation thresholds, making normally tolerable warmth painful.
Nociception is neural detection and signalling of potentially damaging stimuli. Pain is the conscious perception that emerges after central processing; they are related but not identical.
