本实验在多种动物上观察了烟碱急性和慢性耐受现象,并分析其作用机理。 中枢N受体激动剂烟碱小剂量(<0.5mg/kg iv)引起兔、大鼠和小鼠脑电去同步化,大剂量(>1.0mg/kg iv)诱发行为惊厥伴脑电癫痫波,且为中枢N拮抗剂美加明(0.2～0.5mg/kg iv)对抗,而不为M拮抗剂阿托品对抗。提示烟碱诱发惊厥与激动中枢N受体有关。 在大鼠和小鼠上,烟碱0.5mg/kg iv 10min后,脑电恢复正常,这时烟碱1.0～5.0mg/kg iv不能诱发癫痫波。烟碱0.1mg/kg iv仅引起兔脑电去同步化,间隔5min,连续iv 6次后,0.1mg/kg烟碱已基本上不影响脑电,这时增加剂量至1.0～1.5mg/kg(在正常兔上能诱发癫痫波),也不能引起癫痫波。因此,以在清醒脑 In this experiment, acute and chronic nicotine tolerance was observed in a variety of animals, and its mechanism of action was analyzed. Small doses of central N receptor agonist nicotine (<0.5 mg / kg iv) induced depolarization of EEG in rabbits, rats and mice, induced convulsions at high doses (> 1.0 mg / kg iv) with epileptic EEG , And was antagonized by the central N antagonist, mecamylamine (0.2-0.5 mg / kg iv), but not the M antagonist atropine. Tip nicotine-induced convulsion and central nervous system N receptor. In rats and mice, nicotine 0.5mg / kg iv 10min, EEG returned to normal, then nicotine 1.0 ~ 5.0mg / kg iv can not induce epileptic waves. Nicotine 0.1mg / kg iv only caused the EEG deynchronization, interval 5min, continuous iv 6 times, 0.1mg / kg nicotine basically does not affect the EEG, then increase the dose to 1.0 ~ 1.5mg / kg (In normal rabbits can induce epileptic waves), can not cause epileptic waves. So, in the awake brain