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麻醉剂丙泊酚和氯胺酮可抑制可卡因诱导的大鼠前脑egr-1基因表达。

The anesthetics propofol and ketamine inhibit cocaine-induced egr-1 gene expression in rat forebrain.

作者信息

Jouvert Peggy, Pain Laure, Aunis Dominique, Zwiller Jean

机构信息

INSERM U338, Centre de Neurochimie, 5 rue Blaise Pascal, 67084 Strasbourg, Cedex, France.

出版信息

Eur J Pharmacol. 2002 Aug 9;449(3):239-43. doi: 10.1016/s0014-2999(02)02035-6.

Abstract

Acute cocaine injection to rats is known to induce the expression of immediate early genes in the forebrain, the effect being primarily mediated by the dopaminergic system. We examined the effect of the anesthetics ketamine and propofol on cocaine-induced egr-1 mRNA expression. Using in situ hybridization, we show that both compounds did not induce egr-1 gene by themselves, but were able to dose-dependently reduce cocaine-induced egr-1 mRNA synthesis in the nucleus accumbens, caudate-putamen and cingulate cortex. Our data suggest that in addition to glutamate NMDA receptors, propofol may act via GABA(A) receptors or ion channels.

摘要

已知向大鼠急性注射可卡因会诱导前脑中即刻早期基因的表达,这种效应主要由多巴胺能系统介导。我们研究了麻醉剂氯胺酮和丙泊酚对可卡因诱导的egr-1 mRNA表达的影响。通过原位杂交,我们发现这两种化合物自身不会诱导egr-1基因,但能够剂量依赖性地降低可卡因诱导的伏隔核、尾状核-壳核和扣带回皮质中egr-1 mRNA的合成。我们的数据表明,除了谷氨酸NMDA受体外,丙泊酚可能通过GABA(A)受体或离子通道发挥作用。

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