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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.

DOI:10.1016/s0014-2999(02)02035-6
PMID:12167465
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。

相似文献

1
The anesthetics propofol and ketamine inhibit cocaine-induced egr-1 gene expression in rat forebrain.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。
Eur J Pharmacol. 2002 Aug 9;449(3):239-43. doi: 10.1016/s0014-2999(02)02035-6.
2
Inhibitory effect of propofol on ketamine-induced c-Fos expression in the rat posterior cingulate and retrosplenial cortices is mediated by GABAA receptor activation.丙泊酚对氯胺酮诱导的大鼠后扣带回和压后皮质中c-Fos表达的抑制作用是由GABAA受体激活介导的。
Acta Anaesthesiol Scand. 2003 Mar;47(3):284-90. doi: 10.1034/j.1399-6576.2003.00040.x.
3
Ketamine and propofol in combination induce neuroapoptosis and down-regulate the expression of N-methyl-D-aspartate glutamate receptor NR2B subunit in rat forebrain culture.氯胺酮和丙泊酚联合使用可诱导大鼠前脑培养物中的神经细胞凋亡,并下调N-甲基-D-天冬氨酸谷氨酸受体NR2B亚基的表达。
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Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex.丙泊酚抑制氯胺酮诱导的大鼠后扣带回皮质中c-fos的表达。
Anesth Analg. 1998 Dec;87(6):1416-20. doi: 10.1097/00000539-199812000-00040.
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Propofol and ketamine-induced anesthetic depth-dependent decrease of CaMKII phosphorylation levels in rat hippocampus and cortex.丙泊酚和氯胺酮诱导大鼠海马体和皮质中钙/钙调蛋白依赖性蛋白激酶II(CaMKII)磷酸化水平随麻醉深度降低。
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[Interactions of intravenous anesthetics with cerebral alpha-2-adrenoceptors].[静脉麻醉药与脑α-2肾上腺素能受体的相互作用]
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Differential rat brain expression of EGR proteins and of the transcriptional corepressor NAB in response to acute or chronic cocaine administration.大鼠脑内早期生长反应(EGR)蛋白和转录共抑制因子NAB在急性或慢性给予可卡因后的差异表达。
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Ketamine and propofol have opposite effects on postanesthetic sleep architecture in rats: relevance to the endogenous sleep-wakefulness substances orexin and melanin-concentrating hormone.氯胺酮和丙泊酚对大鼠麻醉后睡眠结构有相反作用:与内源性睡眠-觉醒物质食欲素和促黑素细胞激素的相关性
J Anesth. 2016 Jun;30(3):437-43. doi: 10.1007/s00540-016-2161-x. Epub 2016 Mar 16.
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Ketamine, but not propofol, anaesthesia is regulated by metabotropic glutamate 5 receptors.氯胺酮麻醉受代谢型谷氨酸受体5调控,而丙泊酚麻醉则不然。
Br J Anaesth. 2006 May;96(5):597-601. doi: 10.1093/bja/ael046. Epub 2006 Mar 10.
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Tumor necrosis factor-alpha reduces ketamine- and propofol-induced anesthesia time in rats.肿瘤坏死因子-α可缩短大鼠氯胺酮和丙泊酚诱导的麻醉时间。
Anesth Analg. 2002 Oct;95(4):952-5, table of contents. doi: 10.1097/00000539-200210000-00030.

引用本文的文献

1
Propofol induces MAPK/ERK cascade dependant expression of cFos and Egr-1 in rat hippocampal slices.丙泊酚诱导大鼠海马切片中cFos和Egr-1的丝裂原活化蛋白激酶/细胞外信号调节激酶(MAPK/ERK)级联依赖性表达。
BMC Res Notes. 2010 Jul 17;3:201. doi: 10.1186/1756-0500-3-201.
2
Propofol induces ERK-dependant expression of c-Fos and Egr-1 in neuronal cells.丙泊酚诱导神经元细胞中c-Fos和Egr-1的细胞外信号调节激酶依赖性表达。
Neuroreport. 2009 May 6;20(7):657-62. doi: 10.1097/WNR.0b013e328329a449.
3
Anticonvulsant efficacy of drugs with cholinergic and/or glutamatergic antagonism microinfused into area tempestas of rats exposed to soman.
将具有胆碱能和/或谷氨酸能拮抗作用的药物微量注入暴露于梭曼的大鼠的颞叶区域后的抗惊厥效果。
Neurochem Res. 2008 Feb;33(2):348-54. doi: 10.1007/s11064-007-9429-3. Epub 2007 Aug 21.