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.
The article deals with the study of the possibility to use free-living soil nematode C. elegans in researches of anthelmintic activity of plant raw material. A. sativum juice and aqueous extract of T. vulgare flowers were used in experiments. It is shown that both A. sativum juice and tansy flowers extract caused dose-dependent disturbances of C. elegans swimming motor program. These disturbances are similar with disturbances caused by agonist of cholinoreceptors levamisole. Therefore, the target of A. sativum juice and T. vulgare extract action is C. elegans cholinergic system. The mechanism of toxic action of A. sativum and T. vulgare on C. elegans organism consists in hyperactivation of nicotinic cholinoreceptors. The possibility of quick adaptation of C. elegans nicotinic cholinoreceptors to active components of tansy flowers extract was revealed. Soil nematode C. elegans may be used for investigation of anthelmintic activity of A. sativum and T. vulgare for the purpose of identification of secondary metabolites responsible for the toxic action on helminths.
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