论文部分内容阅读
哺乳动物缺氧主要通过颈动脉体 (CB)化学感受性反射导致肺通气量增加 ,但感受器细胞释放何种神经递质介导兴奋性化学传递仍存在争议。本工作利用鼠离体灌流颈动脉体 -窦神经标本及鼠颈动脉体化学感受器细胞 ( 型细胞 ,球型细胞 )与岩神经节细胞 (PNs)共培养建立的功能性化学突触模型 ,研究了乙酰胆碱 (ACh)在介导缺氧刺激 CB化学感受器兴奋传递中的作用。结果发现胆碱能 N受体 (n ACh R)阻断剂mecamylamine和 hexamethonium抑制离体颈动脉体 -窦神经标本细胞自发放电及缺氧诱发电位。穿孔膜片(perforated- patch)钳记录证明 mecamylamine(2 μmol/L)能部分地抑制共培养 PNs自发性突触后电位和缺氧诱发的去极化。应用乙酰胆碱酯酶 (ACh E)抑制剂毒扁豆碱 (eserine,1 0 0 μmol/L)加强缺氧诱发的 PNs去极化活动。提示鼠颈动脉体化学感受器及传入神经节细胞都表达 n ACh R,缺氧时颈动脉体化学感受器细胞可通过释放 ACh,发挥其兴奋性化学传递作用
Mammalian hypoxia leads to increased lung ventilation mainly through carotid body chemoreceptor (CB) chemosensory reflexes, but it remains controversial whether neurotransmitters are released by the sensor cells to mediate excitatory chemical delivery. In this study, a functional chemical synapse model was established by co-culture of rat carotid sinusoids and rat carotid body chemoreceptor cells (type cells, globular cells) and petrocarotid ganglion cells (PNs) The role of acetylcholine (ACh) in mediating hypoxia-stimulated CB chemoreceptor excitability transmission. The results showed that nACh R blockers, mecamylamine and hexamethonium, inhibited spontaneous discharge and hypoxia-evoked potentials in isolated rat carotid sinusoids. Perforated-patch clamp recordings demonstrated that mecamylamine (2 μmol / L) partially inhibited spontaneous postsynaptic potential and hypoxia-induced depolarization in co-cultured PNs. Hypoxia-evoked depolarization of PNs was potentiated by eserine (100 μmol / L), an ACh E inhibitor. Suggesting that nAChR is expressed in the carotid body chemoreceptor and afferent ganglion cells in rat carotid body, and chemotactic effect of carotid body chemoreceptor can be released by releasing ACh