Serotonin inhibition of synaptic transmission:: Gαo decreases the abundance of UNC-13 at release sites
Serotonin inhibition of synaptic transmission:: Gαo decreases the abundance of UNC-13 at release sites
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DOI：
10.1016/s0896-6273(00)80835-1
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发表时间：
1999-09-01
期刊：
影响因子：
16.2
通讯作者：
Kaplan, JM
中科院分区：
文献类型：
--
作者：
Nurrish, S;Ségalat, L;Kaplan, JM
我们发现，血清素抑制突触传递在C。elegans神经肌肉接头，我们描述了一个信号通路，介导这种效果。通过测量完整动物对乙酰胆碱酯酶抑制剂涕灭威的敏感性，分析了运动神经元释放乙酰胆碱的情况。通过该试验，外源性5-羟色胺抑制乙酰胆碱释放，而5-羟色胺拮抗剂刺激释放。5-羟色胺对突触传递的影响是由果阿-1（一种G α（o）亚基）和DGK-1（一种甘油二酯[DAG]激酶）介导的，这两种物质都作用于腹侧脊髓运动神经元。缺乏果阿-1 Got的突变体，在运动神经元神经末梢积累了异常高水平的DAG结合蛋白β-13，这表明5-羟色胺通过减少β-13在释放位点的丰度来抑制突触传递。
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.