中枢N受体对M受体介导体温降低作用的调节

Modulation of central nicotinic receptor on muscarinic receptor-mediated hypothermia

在清醒大鼠上，可进中枢的Ｎ受体拮抗剂美加明可对抗Ｎ受体激动剂烟碱降低体温的作用，增强Ｍ受体激动剂氧化震颤素降低体温的作用；不进中枢的外周Ｎ受体拮抗剂六甲溴铵不影响烟碱和氧化震颤素的上述作用．每天３次ｓｃ烟碱２．５ｍｇ·ｋｇ－１，连续７ｄ，大鼠对烟碱降低体温的作用产生慢性耐受后，氧化震颤素降低体温的作用无显著变化．提示以体温变化为指标，美加明封闭中枢Ｎ受体功能后，中枢Ｍ受体对其激动剂的敏感性增强；反复给予烟碱诱导中枢Ｎ受体功能失敏后，中枢Ｍ受体对其激动剂的敏感性无显著变化．

In conscious rats, the hypothermic effects of nicotine could be prevented by central nicotinic antagonist mecamylamine rather than by peripheral nicotinic antagonist hexamethonium and muscarinic antagonist atropine and methylatropine. The hypothermic effects of muscarinic agonist oxotremorine could be prevented by central muscarinic antagonist atropine rather than by peripheral muscarinic antagonist methylatropine, and could be potentiated by mecamylamine rather than by hexamethonium. In addition, chronic tolerance to nicotine's effects for producing hypothermia was developed by repeated administration with nicotine at a dose of 2 5 mg/kg sc 3 doses a day for 7 days, and the hypothermic effects of oxotremorine remained unchanged. It indicated that the sensitivity of brain muscarinic receptor to its agonist for producing hypothermia could be potentiated with brain nicotinic receptor blockade by mecamylamine rather than with brain nicotinic receptor desensitization by nicotine.