Synaptic Transmission
Neural communication occurs through two sequential processes: electrical signalling within individual neurons (the action potential), and chemical signalling between neurons at synapses. Together, these mechanisms allow the rapid, precise transmission of information across the ~86 billion neurons of the human brain and throughout the body.
The action potential is an all-or-none electrical event generated at the axon hillock when summated synaptic inputs depolarise the membrane to threshold (~−55 mV). Voltage-gated Na+ channels open, driving rapid Na+ influx and depolarisation to approximately +40 mV. The Na+ channel inactivation gates then close (absolute refractory period), and voltage-gated K+ channels open, driving K+ efflux and repolarisation. A brief afterhyperpolarisation (relative refractory period) follows before the resting potential (−70 mV) is restored by the Na+/K+ ATPase. The action potential propagates along the axon — in myelinated fibres via saltatory conduction (jumping from node of Ranvier to node of Ranvier), reaching velocities of 70–120 m/s.
At chemical synapses, the arriving action potential opens voltage-gated Ca2+ channels in the presynaptic terminal. Ca2+ influx triggers synaptotagmin-mediated SNARE complex formation, driving synaptic vesicle fusion with the presynaptic membrane and neurotransmitter exocytosis into the ~20 nm synaptic cleft. Neurotransmitter molecules diffuse across and bind to postsynaptic receptors: ionotropic (ligand-gated ion channel) receptors produce fast, direct changes in membrane potential (milliseconds); metabotropic (G-protein-coupled) receptors activate second-messenger cascades for slower, modulatory effects.
Postsynaptic potentials are graded (not all-or-none). EPSPs (excitatory postsynaptic potentials) depolarise the membrane toward threshold — typically generated by glutamate on AMPA receptors (Na+ influx). IPSPs (inhibitory postsynaptic potentials) hyperpolarise or stabilise the membrane — typically generated by GABA on GABA-A receptors (Cl− influx). The neuron integrates thousands of simultaneous inputs through temporal summation (successive EPSPs from one synapse) and spatial summation (simultaneous EPSPs from multiple synapses), with the algebraic sum evaluated at the axon hillock: if net depolarisation exceeds threshold, an action potential fires. Neurotransmitter action is terminated by reuptake transporters (SERT, DAT, NET, GAT, EAATs), enzymatic degradation (acetylcholinesterase for ACh; MAO and COMT for monoamines), and diffusion.
Frequently Asked Questions
What is an action potential and why is it "all-or-none"?
An action potential is a transient, self-propagating reversal of membrane polarity. When depolarisation at the axon hillock reaches threshold (~−55 mV), a positive feedback cascade opens voltage-gated Na+ channels — Na+ rushes in, driving the membrane to ~+40 mV. This is followed by Na+ channel inactivation and K+ channel opening, which repolarise the membrane. It is "all-or-none" because the Na+ channel opening is regenerative: once threshold is reached, the full amplitude is always the same regardless of stimulus strength. Sub-threshold stimuli produce only graded potentials that decay without propagation. Information is encoded in firing frequency, not amplitude.
What triggers neurotransmitter release at a synapse?
The action potential arriving at the presynaptic terminal opens voltage-gated Ca2+ channels. Ca2+ influx is the essential trigger: Ca2+ binds to synaptotagmin on docked synaptic vesicles, facilitating SNARE protein complex formation, which drives vesicle membrane fusion with the presynaptic plasma membrane (exocytosis). Neurotransmitter is then released into the synaptic cleft. Blocking Ca2+ entry (e.g., with Mg2+ at NMDA receptors, or with ω-conotoxins) abolishes NT release. The coupling of Ca2+ influx to exocytosis occurs within fractions of a millisecond.
What is the difference between an EPSP and an IPSP?
Both are graded postsynaptic potentials. An EPSP (excitatory postsynaptic potential) is a transient depolarisation that moves the membrane potential toward firing threshold — generated by glutamate on AMPA receptors (Na+ influx) or ACh on nicotinic receptors. An IPSP (inhibitory postsynaptic potential) is a transient hyperpolarisation or conductance increase that moves the membrane away from threshold — generated by GABA on GABA-A receptors (Cl− influx) or glycine. Neurons summate thousands of EPSPs and IPSPs simultaneously: if the net result at the axon hillock exceeds threshold, an AP fires.
How is neurotransmitter action terminated?
Three main mechanisms: (1) Reuptake: transporter proteins (SERT for serotonin, DAT for dopamine, NET for noradrenaline, GAT for GABA, EAATs for glutamate) actively remove NT from the cleft into the presynaptic terminal or glia for reuse. (2) Enzymatic degradation: acetylcholinesterase cleaves ACh in the cleft; MAO and COMT degrade monoamines intracellularly. (3) Diffusion: NT disperses from the cleft. These are the primary drug targets in psychiatry: SSRIs block SERT; SNRIs block SERT and NET; cocaine blocks DAT; acetylcholinesterase inhibitors (donepezil) used in Alzheimer's disease.
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Sources
Last reviewed: 8 August 2026
- 1.
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2013). Principles of Neural Science (5th ed.). McGraw-Hill.
TextbookStandard neuroscience reference; comprehensive coverage of membrane biophysics, action potentials, and synaptic transmission.
- 2.
Hodgkin, A. L., & Huxley, A. F. (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. Journal of Physiology, 117(4), 500–544.
Primary studyNobel Prize-winning paper describing the ionic mechanisms of the action potential in the squid giant axon — the foundation of modern electrophysiology.
- 3.
Katz, B. (1969). The Release of Neural Transmitter Substances. Liverpool University Press.
Primary studyKatz's Nobel lecture; established the quantal nature of neurotransmitter release and the role of Ca2+ in vesicle fusion.
- 4.
Bear, M. F., Connors, B. W., & Paradiso, M. A. (2016). Neuroscience: Exploring the Brain (4th ed.). Wolters Kluwer.
TextbookAccessible undergraduate text; clear coverage of action potentials, synaptic transmission, and neurotransmitter systems.