Topic overview

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When an action potential reaches a presynaptic terminal, voltage-gated calcium channels open. Calcium binds synaptotagmin and triggers SNARE-mediated vesicle fusion, releasing neurotransmitter into the cleft. The postsynaptic response depends on receptor subtype: ionotropic receptors produce rapid effects, whereas G-protein-coupled receptors act more slowly. Signals end through reuptake, enzymatic degradation, or diffusion. Release is further shaped by autoreceptor feedback, retrograde messengers, and the availability and recycling of vesicles. Longer-term changes in receptor density contribute to synaptic plasticity. The topic also connects these steps to pharmacological modulation and to toxins that disrupt SNARE-dependent release. Together, these mechanisms provide a framework for understanding how synapses transmit and regulate signals.