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首页> 外文期刊>Environment and Natural Resources Research >Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs
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Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

机译：热疗诱导的秀丽隐杆线虫乙酰胆碱缺乏可通过ACh-酯酶抑制或激活GAR-3 mAChRs来补偿

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The nervous system is a target of hyperthermic failure of animal behavior. Caenorhabditis elegans can be used as an excellent model organism to investigate mechanisms underlying thermotolerance of nervous system. Inhibition of ACh-esterase by neostigmine produces rise in thermotolerance of C. elegans swimming induced by mechanical stimulus at constant temperature 36 °C. Protection of C. elegans behavior against heat stress by neostigmine indicates that hyperthermia induces ACh deficiency in the C. elegans nervous system which is one of the causes of hyperthermic failure of behavior. Activation of mAChRs by pilocarpine or oxotremorine M elevates behavior thermotolerance similarly with neostigmine while inhibition of these receptors by atropine has opposite effect. These results suggest that ACh protects C. elegans behavior against hyperthermia by binding with mAChRs. It is known that three G-protein coupled ACh receptors of C. elegans (GAR-1, GAR-2 and GAR-3) have sequence homology with five known subtypes of mammalian mAChRs. To identify mAChRs responsible for regulation of behavior response to hyperthermia we investigated effects of loss-of-function mutations in gar-1 , gar-2 and gar-3 genes on the sensitivity of behavior thermotolerance to neostigmine and pilocarpine. Among them only loss-of-function gar-3 mutation caused insensitivity of C. elegans behavior thermotolerance to neostigmine and pilocarpine. Thus it is GAR-3 mAChR that mediates rise in behavior thermotolerance produced by ACh-esterase inhibitor neostigmine or agonists of mammalian mAChRs.
机译：神经系统是动物行为高温衰竭的目标。秀丽隐杆线虫可以用作研究神经系统热耐受机制的优秀模型生物。新斯的明对ACh-酯酶的抑制作用导致线虫游泳的耐热性升高，这是由在恒定温度36°C的机械刺激诱导的。通过新斯的明保护线虫行为免受热应激的作用表明，高热诱导线虫神经系统中的ACh缺乏，这是行为过热失败的原因之一。毛果芸香碱或oxotremorine M对mAChRs的激活与新斯的明类似地提高了行为耐受性，而阿托品对这些受体的抑制作用却相反。这些结果表明，ACh通过与mAChRs结合来保护秀丽隐杆线虫对高温的行为。已知秀丽隐杆线虫的三个G蛋白偶联的ACh受体（GAR-1，GAR-2和GAR-3）与哺乳动物mAChR的五个已知亚型具有序列同源性。为了鉴定负责调节对高热行为反应的mAChR，我们研究了gar-1，gar-2和gar-3基因功能缺失突变对行为耐热性对新斯的明和毛果芸香碱敏感性的影响。其中只有功能丧失的gar-3突变引起线虫行为耐热性对新斯的明和毛果芸香碱不敏感。因此，由GAR-3 mAChR介导由ACh-酯酶抑制剂新斯的明或哺乳动物mAChRs激动剂产生的行为耐热性的升高。

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