Serotonin inhibition of synaptic transmission: Galpha(0) decreases the abundance of UNC-13 at release sites.

Abstract:

:We show that serotonin inhibits synaptic transmission at C. elegans neuromuscular junctions, and we describe a signaling pathway that mediates this effect. Release of acetylcholine from motor neurons was assayed by measuring the sensitivity of intact animals to the acetylcholinesterase inhibitor aldicarb. By this assay, exogenous serotonin inhibited acetylcholine release, whereas serotonin antagonists stimulated release. The effects of serotonin on synaptic transmission were mediated by GOA-1 (a Galpha0 subunit) and DGK-1 (a diacylglycerol [DAG] kinase), both of which act in the ventral cord motor neurons. Mutants lacking goa-1 G(alpha)0 accumulated abnormally high levels of the DAG-binding protein UNC-13 at motor neuron nerve terminals, suggesting that serotonin inhibits synaptic transmission by decreasing the abundance of UNC-13 at release sites.

journal_name

Neuron

journal_title

Neuron

authors

Nurrish S,Ségalat L,Kaplan JM

doi

10.1016/s0896-6273(00)80835-1

subject

Has Abstract

pub_date

1999-09-01 00:00:00

pages

231-42

issue

1

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(00)80835-1

journal_volume

24

pub_type

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