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戊巴比妥、氟烷和氯胺酮对大鼠海马CA1锥体细胞抑制性突触后电流的延长作用。

Prolongation of inhibitory postsynaptic currents by pentobarbitone, halothane and ketamine in CA1 pyramidal cells in rat hippocampus.

作者信息

Gage P W, Robertson B

出版信息

Br J Pharmacol. 1985 Jul;85(3):675-81. doi: 10.1111/j.1476-5381.1985.tb10563.x.

DOI:10.1111/j.1476-5381.1985.tb10563.x
PMID:2992670
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1916506/
Abstract

Spontaneous inhibitory postsynaptic currents (i.p.s.cs) were recorded in voltage-clamped CA1 neurones in rat hippocampal slices. The exponential decay of i.p.s.cs was prolonged by concentrations of sodium pentobarbitone as low as 50 microM. With concentrations up to 100 microM, there was no change in the amplitude or rise time of the currents but current amplitude was depressed at 200 microM. The prolongation of currents increased with drug concentration within the range tested (50 to 200 microM). Halothane, at concentrations from 1 to 5%, also increased the time constant of decay of i.p.s.cs. The effect increased with concentration and was fully reversible. Ketamine, at a concentration of 0.5 mM, increased the time constant of decay of i.p.s.cs by 50 to 80% and the effect was reversible. Ethanol (10-200 mM), nitrous oxide (75-80%), and caffeine (10 microM-5 mM) had no detectable effect on the i.p.s.cs. It is suggested that pentobarbitone, halothane and ketamine increase the time constant of decay of the i.p.s.cs by stabilizing the open state of channels activated by gamma-aminobutyric acid.

摘要

在大鼠海马切片中,对电压钳制的CA1神经元记录自发性抑制性突触后电流(i.p.s.cs)。低至50微摩尔浓度的戊巴比妥钠可延长i.p.s.cs的指数衰减。浓度高达100微摩尔时,电流的幅度或上升时间没有变化,但在200微摩尔时电流幅度降低。在所测试的浓度范围(50至200微摩尔)内,电流的延长随药物浓度增加。1%至5%浓度的氟烷也增加了i.p.s.cs的衰减时间常数。这种作用随浓度增加,且完全可逆。0.5毫摩尔浓度的氯胺酮使i.p.s.cs的衰减时间常数增加50%至80%,且该作用可逆。乙醇(10 - 200毫摩尔)、一氧化二氮(75 - 80%)和咖啡因(10微摩尔 - 5毫摩尔)对i.p.s.cs没有可检测到的影响。有人提出,戊巴比妥钠、氟烷和氯胺酮通过稳定由γ-氨基丁酸激活的通道的开放状态来增加i.p.s.cs的衰减时间常数。

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Prolongation of inhibitory postsynaptic currents by pentobarbitone, halothane and ketamine in CA1 pyramidal cells in rat hippocampus.戊巴比妥、氟烷和氯胺酮对大鼠海马CA1锥体细胞抑制性突触后电流的延长作用。
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