Meagher M W, Illich P A, Salinas J A
Texas A & M University, College Station, Texas, 77843-4235, USA.
Neurobiol Learn Mem. 1998 Nov;70(3):374-87. doi: 10.1006/nlme.1998.3871.
Past research indicates that the anticholinergic drug scopolamine disrupts memory and environmentally induced hypoalgesia in rats. The present study examined the impact of the centrally active cholinesterase inhibitor physostigmine, which enhances memory and central cholinergic activity, on brief shock-induced hypoalgesia on the tail-flick test using Sprague-Dawley rats. It is reported that physostigmine (0.1 mg/kg) potentiates the magnitude of this hypoalgesia. Contrary to past research, our results showed that omission of baseline testing did not eliminate hypoalgesia or its potentiation by physostigmine. Similar to its effects on memory, physostigmine (0.04, 0.1, and 0.25 mg/kg) has a nonmonotonic impact on brief shock-induced hypoalgesia; low doses potentiated hypoalgesia (0.1 mg/kg), whereas a high dose (0.25 mg/kg) disrupted it. These results provide further evidence that the cholinergic system indirectly affects pain reactivity by modulating the memory of the aversive event.
过去的研究表明，抗胆碱能药物东莨菪碱会破坏大鼠的记忆以及环境诱导的痛觉减退。本研究使用斯普拉格-道利大鼠，通过甩尾试验，考察了具有增强记忆和中枢胆碱能活性作用的中枢活性胆碱酯酶抑制剂毒扁豆碱对短暂电击诱导的痛觉减退的影响。据报道，毒扁豆碱（0.1毫克/千克）可增强这种痛觉减退的程度。与过去的研究相反，我们的结果显示，省略基线测试并未消除痛觉减退或毒扁豆碱对其的增强作用。与它对记忆的影响类似，毒扁豆碱（0.04、0.1和0.25毫克/千克）对短暂电击诱导的痛觉减退具有非单调影响；低剂量（0.1毫克/千克）增强痛觉减退，而高剂量（0.25毫克/千克）则破坏痛觉减退。这些结果提供了进一步的证据，表明胆碱能系统通过调节对厌恶事件的记忆来间接影响疼痛反应性。
