Autoreceptors, membrane potential and the regulation of transmitter release.
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.
Parnas
H
H
Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Dept of Neurobiology, Alexander Silberman Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel.
Segel
L
L
Dudel
J
J
Parnas
I
I
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*
D015220:Calcium Channels; D018377:Neurotransmitter Agents; D011956:Receptors, Cell Surface; D002118:Calcium