Houser V P
Pharmacol Biochem Behav. 1976 May;4(5):561-8. doi: 10.1016/0091-3057(76)90198-2.
Evidence has been supplied which suggests that a central inhibitory cholingeric (i.e., muscarinic) system may be involved in modulating the aversive qualities of electric shock in the rat. Central cholinergic stimulation via the administration of pilocarpine or arecoline the threshold for grid shock, while central acting anticholinergics (i.e., scopolamine and atropine) produced decrements in the threshold. Peripheral acting anticholinergics (e.g., methyl scopolamine, methyl atropine) were less potent than central acting drugs given in equivalent doses, while peripheral cholinergic stimulants (i.e., neostigmine, carbachol) were inactive. In addition, only the central acting stimulant pilocarpine, and not carbachol, was able to block the decrements noted in response to scopolamine hydrobromide administration. Finally, only arecoline, and not nicotine, was able to elevate the aversive threshold indicating that muscarinic receptor sites are probably involved in mediating the effects of central cholinergic stimulants.
已有证据表明,中枢抑制性胆碱能(即毒蕈碱样)系统可能参与调节大鼠电击的厌恶性。通过给予毛果芸香碱或槟榔碱进行中枢胆碱能刺激可提高网格电击阈值,而中枢作用的抗胆碱能药物(即东莨菪碱和阿托品)则会使阈值降低。外周作用的抗胆碱能药物(如甲基东莨菪碱、甲基阿托品)在等效剂量下比中枢作用药物效力低,而外周胆碱能兴奋剂(即新斯的明、卡巴胆碱)则无活性。此外,只有中枢作用的兴奋剂毛果芸香碱,而不是卡巴胆碱,能够阻断因给予氢溴酸东莨菪碱而引起的阈值降低。最后,只有槟榔碱,而不是尼古丁,能够提高厌恶性阈值,表明毒蕈碱受体部位可能参与介导中枢胆碱能兴奋剂的作用。