Ren J, Harty R F
Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City 73126.
Dig Dis Sci. 1994 May;39(5):1099-106. doi: 10.1007/BF02087564.
The purpose of the present studies was to determine whether autoinhibition of acetylcholine release could be demonstrated in vitro from mucosal/submucosal neurons in rat antrum. Rat antral mucosal/submucosal tissues preloaded with [3H]choline were perifused and [3H]acetylcholine release measured under basal and stimulated conditions. Carbachol inhibited both spontaneous and evoked (electrical field stimulation, KCl) acetylcholine release from rat antral tissues: 1 x 10(-5) M carbachol inhibited basal [3H]ACh release maximally to -38.2 +/- 3.1% (P < 0.001 vs control). The nonselective muscarinic antagonist atropine enhanced both basal and stimulated acetylcholine release and abolished carbachol-induced inhibition of acetylcholine release. Pirenzepine, a muscarinic M1 receptor antagonist, inhibited acetylcholine release and did not alter carbachol-induced inhibition of acetylcholine release. In conclusion, acetylcholine release from rat antral mucosal/submucosal neurons is regulated negatively by a presynaptic feedback mechanism involving M2 and/or M3 receptors, while presynaptic M1 receptors facilitate release of neurotransmitter.
本研究的目的是确定大鼠胃窦黏膜/黏膜下神经元在体外是否能表现出乙酰胆碱释放的自身抑制。预先用[³H]胆碱标记的大鼠胃窦黏膜/黏膜下组织进行灌流，并在基础和刺激条件下测量[³H]乙酰胆碱的释放。卡巴胆碱抑制大鼠胃窦组织中自发的和诱发的（电场刺激、氯化钾）乙酰胆碱释放：1×10⁻⁵ M卡巴胆碱最大程度地抑制基础[³H]乙酰胆碱释放至-38.2±3.1%（与对照组相比，P<0.001）。非选择性毒蕈碱拮抗剂阿托品增强基础和刺激状态下的乙酰胆碱释放，并消除卡巴胆碱诱导的乙酰胆碱释放抑制。哌仑西平，一种毒蕈碱M1受体拮抗剂，抑制乙酰胆碱释放，且不改变卡巴胆碱诱导的乙酰胆碱释放抑制。总之，大鼠胃窦黏膜/黏膜下神经元的乙酰胆碱释放通过涉及M2和/或M3受体的突触前反馈机制受到负调节，而突触前M1受体促进神经递质释放。
