G protein betagamma subunit-mediated presynaptic inhibition: regulation of exocytotic fusion downstream of Ca2+ entry.

Blackmer T, Larsen EC, Takahashi M, Martin TF, Alford S, Hamm HE
Science. 2001 292 (5515): 293-7

PMID: 11303105 · DOI:10.1126/science.1058803

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 betagamma subunits (Gbetagamma) mimics serotonin's inhibitory effect on neurotransmission. Release of free Gbetagamma was critical for this effect because a Gbetagamma scavenger blocked serotonin's effect. Gbetagamma had no effect on fast, action potential-evoked intracellular Ca2+ release that triggered neurotransmission. Inhibition of neurotransmitter release by serotonin was still seen after blockade of all classical Gbetagamma effector pathways. Thus, Gbetagamma blocked neurotransmitter release downstream of Ca2+ entry and may directly target the exocytotic fusion machinery at the presynaptic terminal.

MeSH Terms (26)

Action Potentials Animals Antigens, Surface Axons beta-Adrenergic Receptor Kinases Calcium Calcium Channels Cyclic AMP-Dependent Protein Kinases Excitatory Postsynaptic Potentials Exocytosis GTP-Binding Protein beta Subunits GTP-Binding Protein gamma Subunits Heterotrimeric GTP-Binding Proteins Ion Channel Gating Lampreys Membrane Proteins Microinjections Nerve Tissue Proteins Neural Inhibition Presynaptic Terminals R-SNARE Proteins Recombinant Fusion Proteins Serotonin Synaptic Transmission Synaptosomal-Associated Protein 25 Syntaxin 1

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