Synaptic transmission !

Mechanism
Exam priority: high

A nerve cell passes its signal to the next one by releasing a chemical messenger across a tiny gap: the synapse.

Updated 2026-11-01

Also called: Chemical synapse, EPSP and IPSP

What it is

Most synapses in the nervous system are chemical. An action potential reaching the axon terminal opens voltage-gated Ca²⁺ channels, Ca²⁺ triggers vesicle fusion and the transmitter crosses a cleft of about 20–40 nm. On the other side it produces an excitatory or inhibitory potential, and the neuron adds these up at its initial segment. Synapses explain one-way conduction, delay, summation, fatigue and plasticity, which is why most drugs that act on the brain act here.

How it works, step by step

The action potential reaches the axon terminal and depolarizes it.
Voltage-gated Ca²⁺ channels open and Ca²⁺ rushes in down a steep gradient.
Ca²⁺ binds synaptotagmin; SNARE proteins (synaptobrevin, syntaxin, SNAP-25) fuse docked vesicles with the membrane.
The transmitter is released by exocytosis and crosses the cleft in a fraction of a millisecond.
It binds postsynaptic receptors: ligand-gated channels open at once, or G protein receptors start second messengers.
The resulting EPSP or IPSP spreads passively and fades with distance and time.
If the summed potential at the initial segment reaches threshold, a new action potential fires.
Reuptake transporters, enzymes or diffusion clear the transmitter and end the signal.

Action potential

Rest −70 mVThreshold −55 mVPeak +35 mVDuration ≈ 1–2 ms

Tap a phase (the pills above or its band) or a refractory period (ARP, RRP) at the base of the plot.

Mainly Na⁺
Mainly K⁺
Rest
Threshold
ARP: absolute refractory period
RRP: relative refractory period

Illustrative model drawn by Durgical from typical values; each cell type has its own time scale and values are approximate, not for clinical decisions.

Reference values (typical neuron)

Parameter	Value	Note
Synaptic cleft width	≈20–40 nm
Synaptic delay	≈0.5 ms	per synapse
Resting membrane potential	≈−65 to −70 mV	neuronal soma
Firing threshold	≈−45 to −55 mV	initial segment
Single unitary EPSP	≈0.1–1 mV	central synapse; many must summate

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Toxins and diseases that act at the synapse

Agent	Target	Result
Botulinum toxin	SNARE proteins in cholinergic terminals	No ACh release: flaccid paralysis
Tetanus toxin	SNARE proteins in spinal inhibitory interneurons	No glycine or GABA release: spasms, trismus
Lambert–Eaton antibodies	Presynaptic voltage-gated Ca²⁺ channels	Less release: weakness that improves briefly with effort
Myasthenia gravis antibodies	Postsynaptic nicotinic ACh receptors	Weakness that worsens with use
Organophosphates	Acetylcholinesterase	ACh accumulates: cholinergic crisis

Clinical notes

High plasma Mg²⁺ competes with Ca²⁺ at the terminal and depresses transmission; loss of the knee jerk is an early sign of magnesium toxicity.
Alkalosis raises neuronal excitability (tingling, tetany, seizures); severe acidosis depresses it, leading to stupor and coma.
Organophosphate insecticides, widely used in Colombian agriculture, block acetylcholinesterase and flood cholinergic synapses.

Test yourself

Think of the answer, then tap the question to see it.

Botulinum and tetanus toxins both cleave SNARE proteins. Why does one cause flaccid and the other spastic paralysis?

Botulinum toxin blocks ACh release at the neuromuscular junction, so muscle cannot be activated. Tetanus toxin travels into the cord and blocks glycine and GABA release from inhibitory interneurons, so motor neurons fire unopposed.

One terminal produces an EPSP of 1 mV, but threshold is 15–20 mV above rest. How can the neuron still fire?

By summation: many terminals active at once (spatial) or one terminal firing so fast that EPSPs overlap before they fade (temporal). The sum at the initial segment decides.

Why does opening Cl⁻ channels inhibit a neuron even when the membrane potential barely changes?

The Cl⁻ equilibrium potential lies near rest, so open Cl⁻ channels hold the membrane there. Any excitatory current leaks out through them (shunting inhibition) and cannot reach threshold.

In Lambert–Eaton syndrome, why does strength improve briefly with repeated effort?

Antibodies reduce presynaptic Ca²⁺ channels. Repeated firing lets Ca²⁺ build up inside the terminal, raising transmitter release enough to restore transmission for a while.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 12.5 Communication Between Neurons (OpenStax (Rice University), 2022); 12.4 The Action Potential (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 46). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.