A steroid anesthetic prolongs inhibitory postsynaptic currents in cultured rat hippocampal neurons
A steroid anesthetic prolongs inhibitory postsynaptic currents in cultured rat hippocampal neurons
复制标题
类固醇麻醉剂可延长培养的大鼠海马神经元的抑制性突触后电流
作者：
N. Harrison;S. Vicini;J. Barker
采用全细胞膜片钳法记录培养大鼠海马神经元，观察甾体全麻alphaxalone （3 α -羟基5 α -孕烷11,20-二酮）对药理作用和生理释放GABA的影响。在麻醉范围内的低微摩尔浓度下，阿尔法霉素增强了GABA引起的Cl-电导反应，并延长了GABA介导的突触后电位。在-40 mV电压箝位下，诱发快速向外突触电流，并以单指数动力学衰减；室温下平均衰减时间常数为24毫秒。Alphaxalone将这些抑制性突触后电流的衰减延长了5- 8倍，但峰值幅度没有增加，生长时间也没有变化。在临床有效浓度下，gaba介导的抑制性突触传导的大量延长可能对阿霉素的麻醉活性有重要贡献。
Whole-cell patch-clamp recordings were made from cultured rat hippocampal neurons to examine the effects of the steroidal general anesthetic alphaxalone (3 alpha-hydroxy 5 alpha-pregnane 11,20-dione) on responses to pharmacologically applied and physiologically released GABA. At low micromolar concentrations in the anesthetic range, alphaxalone potentiated Cl- conductance responses elicited by GABA and also prolonged evoked GABA-mediated postsynaptic potentials. Under voltage clamp at -40 mV, rapid outwardly directed synaptic currents were evoked that decayed with single exponential kinetics; mean decay time constant was 24 msec at room temperature. Alphaxalone prolonged the decay of these inhibitory postsynaptic currents by 5- to 8-fold, with no increase in peak amplitude or change in growth time. This substantial prolongation of GABA-mediated inhibitory synaptic conductance at clinically effective concentrations may contribute significantly to the anesthetic activity of alphaxalone.