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Synaptic transmission converts an electrical signal in a presynaptic neuron into a chemical signal that crosses the synaptic cleft and is reconverted to electrical or biochemical signals in the postsynaptic cell. When an action potential reaches an axon terminal, voltage-gated Ca²⁺ channels open and Ca²⁺ influx triggers exocytosis of neurotransmitter-loaded vesicles. Neurotransmitters diffuse across the ~20 nm cleft and bind to postsynaptic receptors: ionotropic receptors open ion channels directly (fast, milliseconds), while metabotropic receptors activate G-protein cascades (slow, seconds to minutes). The signal is terminated by reuptake into the presynaptic terminal, enzymatic degradation, or diffusion away from the cleft.
Trace the seven-step sequence: AP arrives → Ca²⁺ enters → vesicles dock and fuse → neurotransmitter released → binds receptor → postsynaptic current flows → signal terminated. Compare an excitatory synapse (glutamate → AMPA receptor → Na⁺ influx → depolarization → EPSP) vs. an inhibitory synapse (GABA → GABA-A receptor → Cl⁻ influx → hyperpolarization → IPSP). Explain how spatial and temporal summation at the axon hillock determines whether an action potential fires.
Synaptic transmission is the mechanism by which a neuron converts the electrical signal of an action potential into a chemical message, sends that message across a tiny gap, and allows the receiving cell to convert it back into an electrical or biochemical response. You already understand action potentials — the rapid, all-or-none depolarization that travels down an axon. The synapse is what happens at the end.
When the action potential reaches the axon terminal, it depolarizes voltage-gated Ca²⁺ channels in the terminal membrane, causing Ca²⁺ to rush in from the extracellular space. This calcium influx is the coupling event: it triggers vesicles — tiny membrane-bound packages filled with neurotransmitter molecules — to dock with the terminal membrane and fuse with it, dumping their contents into the synaptic cleft. The cleft is only about 20 nanometers wide, so diffusion across it is nearly instantaneous.
On the other side, neurotransmitter molecules bind to postsynaptic receptors. The outcome depends entirely on the receptor type. Ionotropic receptors (like AMPA for glutamate, or GABA-A for GABA) are ion channels directly — binding the neurotransmitter opens the channel in milliseconds. Metabotropic receptors (like many dopamine receptors) instead activate G-proteins, which then launch slower but longer-lasting intracellular cascades. The ion that flows determines the effect: Na⁺ influx depolarizes (EPSP, excitatory); Cl⁻ influx hyperpolarizes (IPSP, inhibitory). Whether a neurotransmitter is excitatory or inhibitory is determined by the receptor it binds, not its own chemistry — the same GABA molecule can be inhibitory in an adult brain and excitatory in a fetal brain because the Cl⁻ gradient reverses during development.
A critical misconception to discard is the idea that the synapse is just a relay station. Chemical synapses introduce gain control: a single action potential can release more or fewer vesicles depending on recent activity (synaptic facilitation and depression). They introduce modulation: third-party inputs can strengthen or weaken a synapse (the basis of learning and memory, via long-term potentiation). And they enable computation: the postsynaptic neuron integrates hundreds of EPSPs and IPSPs arriving at different times (temporal summation) and different locations (spatial summation), and only fires a new action potential if the net depolarization at the axon hillock reaches threshold.
Signal termination is the final piece. If neurotransmitters stayed in the cleft indefinitely, the postsynaptic cell would never stop firing. Three mechanisms clear the cleft: reuptake transporters pull neurotransmitter back into the presynaptic terminal (the mechanism targeted by SSRIs, which block serotonin reuptake); enzymatic degradation breaks the neurotransmitter down in the cleft (acetylcholinesterase does this for acetylcholine); and simple diffusion dilutes what remains. Each mechanism has different kinetics and can be pharmacologically targeted — which is why understanding synaptic transmission is foundational to neuropharmacology.