Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

摘要: The nervous system is a target of hyperthermic failure animal behavior. Caenorhabditis elegans can be used as an excellent model organism to investigate mechanisms underlying thermotolerance system. Inhibition ACh-esterase by neostigmine produces rise in C. swimming induced mechanical stimulus at constant temperature 36 °C. Protection behavior against heat stress indicates that hyperthermia induces ACh deficiency the which one causes Activation mAChRs pilocarpine or oxotremorine M elevates similarly with while inhibition these receptors atropine has opposite effect. These results suggest protects binding mAChRs. It known three G-protein coupled (GAR-1, GAR-2 and GAR-3) have sequence homology five subtypes mammalian To identify responsible for regulation response we investigated effects loss-of-function mutations gar-1, gar-2 gar-3 genes on sensitivity pilocarpine. Among them only mutation caused insensitivity Thus it GAR-3 mAChR mediates produced inhibitor agonists