大鼠颈上神经节烟碱受体失敏后毒蕈碱受体的活性增强

目的：在单个培养的大鼠颈上交感神经元上研究失敏烟碱受体(N受体)对毒蕈碱受体(M受体)活性的影响．方法：采用全细胞膜片筘技术．结果：对神经元喷射烟碱可激活N受体诱发一内向电流,烟碱持续作用导致N受体快速失敏．氧化震颤素和毛果芸香碱均能激活M受体诱发一外向电流,M受体没有出现失敏现象．长时间持续喷射烟碱使N受体完全失敏后M受体激活所诱发外向电流的幅度与正常相比明显增大,而一旦去除烟碱,失敏的N受体对烟碱的敏感性将会逐步恢复,在此过程中M受体增加的活性也随之消失：另外,失敏的N受体对M受体活性的增强作用还可被美加明阻断．结论：大鼠交感神经元N受体失敏后M受体对其激动剂的反应增强．

Muscarinic receptor activities potentiated by desensitization of nicotinic receptors in rat superior cervical ganglia

AIM: The influences of desensitized nicotinic acetylcholine receptors (nAChR) on the activities of muscarinic acetylcholine receptors (mAChR) were investigated in single cultured rat superior cervical ganglion. METHODS: Whole-cell patch-clamp techniques were used. RESULTS: An inward current was induced by nicotine 80 micromol/L in the sympathetic neurons and desensitized rapidly after the prolonged exposure to nicotine. An outward current was induced by oxotremorine 100 micromol/L or pilocarpine 100 micromol/L and it showed no desensitization after exposure to its agonists. After nAChR desensitized completely, the current evoked by oxotremorine was increased significantly compared with its control. There were (42 38) % (n=8, P<0.05) and (165 66) % (n=5, P<0.01) increases induced by 100 and 500 micromol/L oxotremorine, respectively. Similar results were also obtained from pilocarpine and the current evoked by 100 micromol/L pilocarpine increased by (66 33) % (n=6, P<0.05) after nAChR desensitization. Once nicotine was removed, nAChR recovered from desensitization gradually and the enhanced mAChR activity also subsided along with it. Furthermore, the facilitatory effect of desensitized nAChR on mAChR activity could be prevented by mecamylamine. CONCLUSION: The activities of mAChR to its agonists were potentiated by the desensitization of nAChR in rat sympathetic neurons