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机构地区:[1]同济医科大学实验医学研究中心,武汉430030
出 处:《生理学报》1998年第1期37-42,共6页Acta Physiologica Sinica
基 金:国家自然科学基金!资助项目No.39370239
摘 要:在新鲜分离大鼠背根神经节(DRG)的56个细胞标本上,应用全细胞膜片箝技术进行记录。胞外加缓激肽(BK,10-6~10-4mol/L)引起的DRG细胞膜反应结果如下:(1)71.4%的细胞为内向电流,其电流反应的幅值具有明显的浓度依赖性;(2)12.5%的细胞为外向电流;(3)16.1%的细胞未引起可检测的膜反应。单独给予ATP(10-6~10-3mol/L)在大多数受检细胞(54/56)引起一浓度依赖性内向电流,并有明显的去敏感现象。预加BK30S后再加ATP,则ATP激活电流明显增强,其电流幅值的增强作用依赖于BK及ATP浓度。BK对ATP激活电流的增强作用以增强其峰电流为主,对稳态部分增强不明显。实验观察了BK增强作用的时程,在检测的4例细胞中发现BK均于预加30s后起效,作用持续20min以上。本文结果提示:BK在初级感觉神经元水平对ATP引起的兴奋性反应可能起到一种易化作用。Modulation of bradykinin(BK)on ATP-activated membrane currents in the isolated rat dorsal root ganglion(DRG)neurons was investigated using whole-cell patch-clamp technique.In 56 neurons examined,BK(10-6~1O-4 mol/L)-induced responses were as follow:(1)inward current (40/56);(2) outward current(7/56);(3)no responses(9/56).In the majority of the neurons examined,ATP(l0-6~1O-3 mol/L)astivated a concentration-dependent inward current with obvious desensitization.ATP activated current was potentiated markedly by preapplication of BK.The enhancement of BK was depndent on the concentration of BK and ATP.It was found that BK potentiated the peak value of ATP-activated currents predominately while the steady state value was not affected obviously.The onset of BK potentiation of ATP-activated currents needed preincubation of BK at least for 3O s and the time of the enhancement lasted over 2O min.The results suggest that BK may play a role in the facilitation of the exitatory effect of ATP on primary sensory neurons.
关 键 词:缓激肽 背根神经节 ATP 激活电流 调制 神经元
分 类 号:R338.1[医药卫生—人体生理学] Q516[医药卫生—基础医学]
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