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两个钙通道之间的拮抗关系对秀丽隐杆线虫M4神经肌肉接头处突触传递的调节

Regulation of synaptic transmission at the Caenorhabditis elegans M4 neuromuscular junction by an antagonistic relationship between two calcium channels.

作者信息

Steciuk Mark, Cheong Mi, Waite Christopher, You Young-Jai, Avery Leon

机构信息

Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148.

Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, Virginia 23298-0551.

出版信息

G3 (Bethesda). 2014 Nov 4;4(12):2535-43. doi: 10.1534/g3.114.014308.

Abstract

In wild-type Caenorhabditis elegans, the synapse from motor neuron M4 to pharyngeal terminal bulb (TB) muscles is silent, and the muscles are instead excited by gap junction connections from adjacent muscles. An eat-5 innexin mutant lacking this electrical connection has few TB contractions and is unable to grow well on certain foods. We showed previously that this defect can be overcome by activation of the M4 → TB synapse. To identify genes that negatively regulate synaptic transmission, we isolated new suppressors of eat-5. To our surprise, these suppressors included null mutations in NPQR-type calcium channel subunit genes unc-2 and unc-36. Our results are consistent with the hypothesis that Ca(2+) entry through the NPQR-type channel inhibits synaptic transmission by activating the calcium-activated K(+) channel SLO-1, thus antagonizing the EGL-19 L-type calcium channel.

摘要

在野生型秀丽隐杆线虫中,运动神经元M4与咽终球(TB)肌肉之间的突触是沉默的,相反,这些肌肉是由相邻肌肉的间隙连接激发的。缺乏这种电连接的eat-5连接蛋白突变体几乎没有TB收缩,并且在某些食物上无法良好生长。我们之前表明,这种缺陷可以通过激活M4→TB突触来克服。为了鉴定负向调节突触传递的基因,我们分离了eat-5的新抑制子。令我们惊讶的是,这些抑制子包括NPQR型钙通道亚基基因unc-2和unc-36的无效突变。我们的结果与以下假设一致:通过NPQR型通道进入的Ca(2+)通过激活钙激活钾通道SLO-1来抑制突触传递,从而拮抗EGL-19 L型钙通道。

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