Molecular mechanisms that control initiation and termination of physiological depolarization-evoked transmitter release.

ABSTRACT: Ca(2+) is essential for physiological depolarization-evoked synchronous neurotransmitter release. But, whether Ca(2+) influx or another factor controls release initiation is still under debate. The time course of ACh release is controlled by a presynaptic inhibitory G protein-coupled autoreceptor (GPCR), whose agonist-binding affinity is voltage-sensitive. However, the relevance of this property for release control is not known. To resolve this question, we used pertussis toxin (PTX), which uncouples GPCR from its G(i/o) and in turn reduces the affinity of GPCR toward its agonist. We show that PTX enhances ACh and glutamate release (in mice and crayfish, respectively) and, most importantly, alters the time course of release without affecting Ca(2+) currents. These effects are not mediated

SUBMITTER: Kupchik YM 

PROVIDER: S-EPMC2393753 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature