Conclusion

That impulse-evoked release of neurotransmitters depends on a Ca2+-dependent extrusion from storage vesicles is beyond dispute. However, many details concerning the supply of vesicles that participate in this process, as well as the processes which regulate the docking and fusion of synaptic vesicles with the axolemma, remain uncertain. Nevertheless, it is clear that the amount of transmitter that is released in this

Glutamate

Neuronal o glial proc├Ęs

GABA

Figure 4.13 GABA release by reversed uptake ('retrotransport'). Depolarization of a neuronal, or glial cell process by glutamate, with a concomitant rise in [Na+]i reverses the operation of the GABA uptake carrier, raising [GABA]o. (Modified from Attwell, Barbour and Szatkowski 1993, with permission from the publisher Cell Press)

GABA

Figure 4.13 GABA release by reversed uptake ('retrotransport'). Depolarization of a neuronal, or glial cell process by glutamate, with a concomitant rise in [Na+]i reverses the operation of the GABA uptake carrier, raising [GABA]o. (Modified from Attwell, Barbour and Szatkowski 1993, with permission from the publisher Cell Press)

way is influenced by a network of auto- and heteroceptors. Activation of these receptors is coupled to the release process through their respective second messengers. It is also evident that vesicular exocytosis is not the only process which leads to release of transmitter from nerve terminals. Under certain conditions, axolemma-bound transporters can export transmitters from neurons or even evoke exocytosis. It seems that a range of processes contribute to release of neurotransmitters, all of which could have a vital role in the regulation of neurotransmission.

Was this article helpful?

0 0

Post a comment