氯胺酮对离体蟾蜍椎旁神经节细胞的抑制作用

目的　了解静脉全麻药氯胺酮对交感神经节单个神经元的作用和机制。方法　应用离体蟾蜍椎旁神经节(PVG)细胞内记录技术 ,观察不同浓度的氯胺酮对PVG细胞的膜电学特性、动作电位及兴奋性的影响。结果　对离体PVG灌流 0 .3～ 3.0mmol/L氯胺酮可浓度依赖性地引起轻度去极化反应 (n =2 0 ,P <0 .0 5 ) ,降低直接动作电位的幅度和超射值 (P <0 .0 1) ,延长半幅时程 (P <0 .0 5 ) ,并明显提高动作电位的阈电位水平 (P <0 .0 5 ) ,使刺激电流强度 放电频率关系曲线右移 ,在 3mmol/L浓度减小膜电阻 (P <0 .0 5 ) ,完全取消动作电位的产生。结论　氯胺酮对离体蟾蜍椎旁神经节细胞具有直接的抑制作用

Inhibitory effects of ketamine on paravertebral ganglion neurons of toad in vitro

Objective To evaluate the effects of ketamine,an intravenous anesthetic and NMDA receptor antagonist,on paravertebral ganglion (PVG) neurons of toad (Bufo gargarizans Cantor) in vitro.MethodsIntracellular recordings were obtained from the isolated PVG neurons of toad.ResultsIt was observed that perfusion of ketamine (0.3～3.0 mmol/L,15 min,n=20) concentration-dependently and reversibly depolarized the PVG neurons (P<0.05),decreased the amplitude and overshoot of action potential (P<0.01),but increased the half-width of spike potential (P<0.01).Moreover,the threshold for firing of action potential was significantly raised (P<0.05),and the current intensity-firing frequency relationship (I-F) curve was shifted rightward by bath of ketamine,in which action potentials recorded from 20 neurons were all nullified by ketamine at 3.0 mmol/L.Conclusion Ketamine may exhibit an inhibitory action on the toad PVG neurons directly by suppression of the neuronal excitability and decrease of the spike amplitude of action potential.