神经递质Neurotransmitter

动作电位到达轴突末梢，使电压门控钙通道开放，Ca²⁺ 内流触发突触小泡与细胞膜融合，以胞吐方式释放递质。递质扩散过突触间隙（约 20 nm），与突触后膜受体结合：离子型受体直接开放离子通道，代谢型受体通过 G 蛋白和第二信使起作用。随后递质被酶降解（如乙酰胆碱酯酶水解乙酰胆碱）或被重摄取，使信号终止。

An action potential reaching the axon terminal opens voltage-gated calcium channels; Ca²⁺ entry triggers synaptic vesicles to fuse with the membrane and release transmitter by exocytosis. The transmitter diffuses across the synaptic cleft (about 20 nm) and binds postsynaptic receptors: ionotropic receptors open ion channels directly, while metabotropic receptors act through G proteins and second messengers. The signal ends when the transmitter is broken down by enzymes, such as acetylcholinesterase for acetylcholine, or taken back up.

1921 年奥托·勒维用两颗离体蛙心实验证明，刺激迷走神经释放的“迷走神经物质”能让另一颗心脏减速，后被戴尔鉴定为乙酰胆碱，两人获 1936 年诺贝尔生理学或医学奖。1950 年代卡尔森发现多巴胺是独立的递质，并与帕金森病相关；阿克塞尔罗德研究了去甲肾上腺素的重摄取机制。

In 1921 Otto Loewi showed with two isolated frog hearts that a substance released by stimulating the vagus nerve slowed a second heart; Dale identified it as acetylcholine, and they shared the 1936 Nobel Prize in Physiology or Medicine. In the 1950s Carlsson showed dopamine is a transmitter in its own right and linked it to Parkinson's disease, and Axelrod worked out the reuptake of noradrenaline.

许多药物作用于递质系统：左旋多巴补充多巴胺治疗帕金森病；选择性 5-羟色胺再摄取抑制剂（如氟西汀）治疗抑郁症；苯二氮䓬类增强 GABA 作用；有机磷农药和神经毒剂抑制乙酰胆碱酯酶，阿托品可作为解毒剂。尼古丁、可卡因等成瘾物质也作用于这些系统。

Many drugs target transmitter systems: L-DOPA replaces dopamine in Parkinson's disease, selective serotonin reuptake inhibitors such as fluoxetine treat depression, and benzodiazepines enhance GABA. Organophosphate pesticides and nerve agents inhibit acetylcholinesterase, for which atropine is an antidote. Addictive substances such as nicotine and cocaine also act on these systems.