Autoreceptors, membrane potential and the regulation of transmitter release

Trends Neurosci. 2000 Feb;23(2):60-8. doi: 10.1016/s0166-2236(99)01498-8.

Abstract

It has been suggested that depolarization per se can control neurotransmitter release, in addition to its role in promoting Ca2+ influx. The 'Ca2+ hypothesis' has provided an essential framework for understanding how Ca2+ entry and accumulation in nerve terminals controls transmitter release. Yet, increases in intracellular Ca2+ levels alone cannot account for the initiation and termination of release; some additional mechanism is needed. Several experiments from various laboratories indicate that membrane potential has a decisive role in controlling this release. For example, depolarization causes release when Ca2+ entry is blocked and intracellular Ca2+ levels are held at an elevated level. The key molecules that link membrane potential with release control have not yet been identified: likely candidates are presynaptic autoreceptors and perhaps the Ca2+ channel itself.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Binding Sites
  • Calcium / metabolism
  • Calcium Channels / metabolism
  • Exocytosis*
  • Membrane Potentials
  • Models, Neurological
  • Neurotransmitter Agents / metabolism*
  • Receptors, Cell Surface / metabolism*

Substances

  • Calcium Channels
  • Neurotransmitter Agents
  • Receptors, Cell Surface
  • Calcium