Talking Across the Gap
Neurons rarely touch. Between the axon terminal of one neuron and the dendrite of the next lies a microscopic gap, the synapse (or synaptic cleft). The electrical action potential cannot jump it directly; instead it is converted into a chemical message.
When the action potential reaches the axon terminal, it triggers tiny sacs called vesicles to release neurotransmitters into the synaptic cleft. These chemical messengers drift across and bind to receptor sites on the receiving neuron, like a key fitting a lock. Binding either excites the receiving neuron (nudging it toward firing) or inhibits it (nudging it away). Whether the neuron fires depends on the summed balance of all excitatory and inhibitory signals it receives.
The message must then be cleared so the synapse can reset. The main mechanism is reuptake: the sending neuron reabsorbs the leftover neurotransmitter for reuse. Drugs exploit exactly this machinery. An agonist mimics or boosts a neurotransmitter's effect; an antagonist blocks it. Many antidepressants, for example, block the reuptake of serotonin, leaving more of it active in the synapse.
Common pitfall: picturing the electrical impulse as jumping the synapse itself. It does not. At the synapse the signal switches from electrical to chemical — neurotransmitters carry it across — and only then becomes electrical again in the next neuron.
A: an impulse arrives at the terminal; vesicles fuse and release dots of neurotransmitter into the cleft; dots bind receptors on the far membrane.