SYNAPTIC FUNCTION IS IMPAIRED BUT NOT ELIMINATED IN C-ELEGANS MUTANTS LACKING SYNAPTOTAGMIN
SYNAPTIC FUNCTION IS IMPAIRED BUT NOT ELIMINATED IN C-ELEGANS MUTANTS LACKING SYNAPTOTAGMIN
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DOI：
10.1016/0092-8674(93)90357-v
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发表时间：
1993-07-02
期刊：
影响因子：
64.5
通讯作者：
RAND, JB
中科院分区：
文献类型：
--
作者：
NONET, ML;GRUNDAHL, K;RAND, JB
Synaptotagmin是一种丰富的突触囊泡相关蛋白，被认为参与钙介导的神经递质释放。我们的分子和遗传学结果表明，尽管突触蛋白是秀丽隐杆线虫突触前神经末梢正常功能所必需的，但突触蛋白突变体中仍存在一些神经递质释放。在秀丽隐杆线虫的神经元中，synaptotagmin定位于富含突触的区域，似乎与突触囊泡有关。synaptotagmin基因的突变体，被称为snt-1，表现出严重的行为异常，以突触功能缺陷为特征，包括严重的运动、进食和排便缺陷。这些突变体在胞吐方面有缺陷，因为它们会积累乙酰胆碱，并且对胆碱酯酶抑制剂有抗性，但它们对胆碱能受体激动剂仍然敏感。尽管存在这些胞外缺陷，snt-1突变体能够协调运动，这表明突变体没有完全阻断神经递质释放。
Synaptotagmin is an abundant synaptic vesicle-associated protein proposed to be involved in calcium-mediated neurotransmitter release. Our molecular and genetic results demonstrate that, although synaptotagmin is required for the proper function of the presynaptic nerve terminal in C. elegans, some neurotransmitter release persists in synaptogamin mutants. In C. elegans neurons, synaptotagmin is localized to regions known to be rich in synapses and appears to be associated with synaptic vesicles. Mutants defective in the synaptotagmin gene, called snt-1, exhibit severe behavioral abnormalities that are characteristic of deficiencies in synaptic function, including severe locomotion, feeding, and defecation defects. The mutants are defective in exocytosis, since they accumulate acetylcholine, and are resistant to cholinesterase inhibitors, but they nevertheless remain sensitive to cholinergic receptor agonists. In spite of these exocytic defects, snt-1 mutants are capable of coordinated motor movements, indicating that the mutants do not have a complete block of neurotransmitter release.