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体外实验中全身麻醉药对嗅皮质神经元抑制作用的增强

Potentiation of inhibition by general anaesthetics in neurones of the olfactory cortex in vitro.

作者信息

Scholfield C N

出版信息

Pflugers Arch. 1980 Feb;383(3):249-55. doi: 10.1007/BF00587527.

DOI:10.1007/BF00587527
PMID:7190680
Abstract

Pentobarbitone, phenobarbitone, methohexitone, chloralose and alphaxalone produced 10-fold increases in the duration of an inhibitory post-synaptic conductance (i.p.s.c.) as recorded intracellularly from neurones of the guinea-pig olfactory cortex in vitro. Higher concentrations slightly depolarised these neurones and reduced their input resistance (Ri), presumably a spontaneous activation of the inhibitory conductance. The excitatory potentials were also depressed. Ketamine, halothane and urethane doubled the i.p.s.c. duration. Higher concentrations depressed synaptic activity and the action potential, as did lignocaine. Ketamine also increased Ri. These results confirm the idea that these compounds produce anaesthesia by prolonging inhibition (accompanied by a depression of the e.p.s.p. with some anaesthetics).

摘要

在体外对豚鼠嗅觉皮层神经元进行细胞内记录时,戊巴比妥、苯巴比妥、甲己炔巴比妥、氯醛糖和α-羟孕酮使抑制性突触后电导(i.p.s.c.)的持续时间增加了10倍。更高浓度会使这些神经元轻微去极化并降低其输入电阻(Ri),推测这是抑制性电导的自发激活。兴奋性电位也受到抑制。氯胺酮、氟烷和乌拉坦使i.p.s.c.持续时间加倍。更高浓度会抑制突触活动和动作电位,利多卡因也是如此。氯胺酮还会增加Ri。这些结果证实了这样一种观点,即这些化合物通过延长抑制作用(一些麻醉剂会伴随兴奋性突触后电位的抑制)来产生麻醉效果。

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