G Protein βγ Subunit-Mediated Presynaptic Inhibition: Regulation of Exocytotic Fusion Downstream of Ca 2+ Entry

Author:

Blackmer Trillium12,Larsen Eric C.3,Takahashi Michiko4,Martin Thomas F. J.3,Alford Simon45,Hamm Heidi E.12

Affiliation:

1. Department of Molecular Pharmacology and Biological Chemistry,

2. Northwestern University Institute for Neuroscience, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611, USA.

3. Department of Biochemistry, University of Wisconsin at Madison, Madison, WI 53706, USA.

4. Department of Physiology,

5. Department of Biological Sciences, University of Illinois at Chicago, 840 West Taylor Street, Chicago, IL 60608, USA.

Abstract

The nervous system can modulate neurotransmitter release by neurotransmitter activation of heterotrimeric GTP–binding protein (G protein)–coupled receptors. We found that microinjection of G protein βγ subunits (Gβγ) mimics serotonin's inhibitory effect on neurotransmission. Release of free Gβγ was critical for this effect because a Gβγ scavenger blocked serotonin's effect. Gβγ had no effect on fast, action potential–evoked intracellular Ca 2+ release that triggered neurotransmission. Inhibition of neurotransmitter release by serotonin was still seen after blockade of all classical Gβγ effector pathways. Thus, Gβγ blocked neurotransmitter release downstream of Ca 2+ entry and may directly target the exocytotic fusion machinery at the presynaptic terminal.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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