title: Autoreceptors, membrane potential and the regulation of transmitter release.
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.
authors.affiliation: Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Dept of Neurobiology, Alexander Silberman Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel.
authors.forename: H
authors.initials: H
authors.lastname: Parnas
authors.forename: L
authors.initials: L
authors.lastname: Segel
authors.forename: J
authors.initials: J
authors.lastname: Dudel
authors.forename: I
authors.initials: I
authors.lastname: Parnas
mesh_terms: D000818:Animals; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D005089:Exocytosis; D008564:Membrane Potentials; D008959:Models, Neurological; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*
chemical_list: D015220:Calcium Channels; D018377:Neurotransmitter Agents; D011956:Receptors, Cell Surface; D002118:Calcium