Neurons communicate with other cells by the release of chemical neurotransmitters, which act transiently on post-synaptic receptors and then must be removed from the synaptic cleft (Fig. 3.15). Transmitter is stored in synaptic vesicles and released on nerve stimulation by the process of exocytosis, following the opening of voltage-gated calcium ion channels in the nerve terminal. Once released, the neu-rotransmitter binds to and stimulates its receptors briefly before being rapidly removed from the synapse, thereby allowing the transmission of a new neuronal message. The most common mode of removal of the neurotransmitter following release is called high-affinity reuptake by the presynaptic terminal. This is a carrier-mediated, sodium-dependent, secondary active transport that uses energy from the Na+/K+- ATPase pump. Other removal mechanisms include enzymatic degradation into a nonactive metabolite in the synapse or diffusion away from the synapse into the extracellular space.
The details of synaptic events in chemical transmission were originally described for PNS synapses. CNS synapses appear to use similar mechanisms, with the important difference that muscle and gland cells are the targets of transmission in peripheral nerves, whereas neurons make up the postsynaptic elements at central synapses. In the central nervous system, glial cells also play a crucial role in remov-
Membrane potential along dendrite
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