Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Trends Neurosci. 2000 Feb;23(2):60-8.

Autoreceptors, membrane potential and the regulation of transmitter release.

Author information

  • 1Otto Loewi Minerva Center for Cellular and Molecular Neurobiology, Dept of Neurobiology, Alexander Silberman Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel.

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.

PMID:
10652546
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk