Serotonin inhibition of synaptic transmission:: Gαo decreases the abundance of UNC-13 at release sites

被引:250
作者
Nurrish, S
Ségalat, L
Kaplan, JM
机构
[1] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA
[2] CNRS, Inst Pharmacol Mol & Cellulaire, F-06560 Valbonne, France
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S0896-6273(00)80835-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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. Fly 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 G alpha(o) subunit) and DGK-1 (a diacylglycerol [DAG] kinase), both of which act in the ventral cord motor neurons. Mutants lacking goa-1 Got, 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.
引用
收藏
页码:231 / 242
页数:12
相关论文
共 47 条
[1]   THE CAENORHABDITIS-ELEGANS UNC-13 GENE-PRODUCT IS A PHOSPHOLIPID-DEPENDENT HIGH-AFFINITY PHORBOL ESTER RECEPTOR [J].
AHMED, S ;
MARUYAMA, IN ;
KOZMA, R ;
LEE, J ;
BRENNER, S ;
LIM, L .
BIOCHEMICAL JOURNAL, 1992, 287 :995-999
[2]   PHARYNX OF CAENORHABDITIS ELEGANS [J].
ALBERTSON, DG ;
THOMSON, JN .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES, 1976, 275 (938) :299-&
[3]   EFFECTS OF STARVATION AND NEUROACTIVE DRUGS ON FEEDING IN CAENORHABDITIS-ELEGANS [J].
AVERY, L ;
HORVITZ, HR .
JOURNAL OF EXPERIMENTAL ZOOLOGY, 1990, 253 (03) :263-270
[4]   The serotonin hypothesis of aggression revisited [J].
Berman, ME ;
Tracy, JI ;
Coccaro, EF .
CLINICAL PSYCHOLOGY REVIEW, 1997, 17 (06) :651-665
[5]   Munc13-1 is a presynaptic phorbol ester receptor that enhances neurotransmitter release [J].
Betz, A ;
Ashery, U ;
Rickmann, M ;
Augustin, I ;
Neher, E ;
Südhof, TC ;
Rettig, J ;
Brose, N .
NEURON, 1998, 21 (01) :123-136
[6]   Mutations in a C-elegans G(q)alpha gene disrupt movement, egg laying, and viability [J].
Brundage, L ;
Avery, L ;
Katz, A ;
Kim, UJ ;
Mendel, JE ;
Sternberg, PW ;
Simon, MI .
NEURON, 1996, 16 (05) :999-1009
[7]   TETRAETHYLAMMONIUM BLOCKADE DISTINGUISHES 2 INACTIVATION MECHANISMS IN VOLTAGE-ACTIVATED K+ CHANNELS [J].
CHOI, KL ;
ALDRICH, RW ;
YELLEN, G .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (12) :5092-5095
[8]   Elevated alcohol consumption in null mutant mice lacking 5-HT1B serotonin receptors [J].
Crabbe, JC ;
Phillips, TJ ;
Feller, DJ ;
Hen, R ;
Wenger, CD ;
Lessov, CN ;
Schafer, GL .
NATURE GENETICS, 1996, 14 (01) :98-101
[9]   Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C-elegans [J].
de Bono, M ;
Bargmann, CI .
CELL, 1998, 94 (05) :679-689
[10]   A GENETIC PATHWAY FOR THE DEVELOPMENT OF THE CAENORHABDITIS-ELEGANS HSN MOTOR NEURONS [J].
DESAI, C ;
GARRIGA, G ;
MCINTIRE, SL ;
HORVITZ, HR .
NATURE, 1988, 336 (6200) :638-646