Qin Wan1, Zhi-Pu Luo, Hai Wang. 1. Institute of Pharmacology and Toxicology, Academy of Military Medical Sciences, Beijing 100850, China.
Abstract
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
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