Scott R W, Goode T L, Raffa R B
Pharmacol Biochem Behav. 1987 Feb;26(2):327-31. doi: 10.1016/0091-3057(87)90126-2.
Intrathecal (IT) administration of pilocarpine (0.25-2.0 micrograms) to mice produced a vigorous and dose-related reciprocal hindlimb scratching response that lasted for 10-15 minutes. Neither the intracerebroventricular administration of pilocarpine at up to 10 times the intrathecal ED90 dose nor the subcutaneous administration of 10 mg/kg pilocarpine caused as robust an effect as IT administration. The reciprocal hindlimb scratching produced by the ED90 dose of pilocarpine (2 micrograms, IT) was antagonized in a dose-related manner by simultaneous IT administration of atropine (ID50 = 0.002 micrograms), methysergide (ID50 = 1.89 micrograms), the substance P antagonist [D-Pro2,D-Trp7,9]-SP (ID50 = 4.94 micrograms), and the putative neurokinin B antagonist [D-Pro2,D-Trp6,8,Nle10]-NK (ID50 = 3.33 micrograms), but not by yohimbine (5 micrograms), phentolamine (2 micrograms), or naloxone (2.5 micrograms). These results suggest that pilocarpine-induced reciprocal hindlimb scratching is mediated spinally, that the effect is produced by an action of pilocarpine on muscarinic receptors in the spinal cord, and that neurokinin, and perhaps 5-HT, mechanisms might also be involved.
向小鼠鞘内注射毛果芸香碱(0.25 - 2.0微克)会引发强烈且与剂量相关的后肢交互抓挠反应,该反应持续10 - 15分钟。脑室内注射高达鞘内ED90剂量10倍的毛果芸香碱,以及皮下注射10毫克/千克的毛果芸香碱,均未产生如鞘内注射那样强烈的效果。鞘内注射ED90剂量的毛果芸香碱(2微克,鞘内注射)所引发的后肢交互抓挠反应,会被同时鞘内注射阿托品(ID50 = 0.002微克)、甲基麦角新碱(ID50 = 1.89微克)、P物质拮抗剂[D - Pro2,D - Trp7,9] - SP(ID50 = 4.94微克)和假定的神经激肽B拮抗剂[D - Pro2,D - Trp6,8,Nle10] - NK(ID50 = 3.33微克)以剂量相关的方式拮抗,但不会被育亨宾(5微克)、酚妥拉明(2微克)或纳洛酮(2.5微克)拮抗。这些结果表明,毛果芸香碱诱导的后肢交互抓挠是由脊髓介导的,该效应是毛果芸香碱作用于脊髓毒蕈碱受体产生的,并且神经激肽以及可能的5 - 羟色胺机制也可能参与其中。