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MK801可诱导大鼠大脑皮质神经元中的即早基因蛋白和脑源性神经营养因子信使核糖核酸。

MK801 induces immediate-early gene proteins and BDNF mRNA in rat cerebrocortical neurones.

作者信息

Hughes P, Dragunow M, Beilharz E, Lawlor P, Gluckman P

机构信息

Department of Pharmacology, School of Medicine, University of Auckland, New Zealand.

出版信息

Neuroreport. 1993 Feb;4(2):183-6. doi: 10.1097/00001756-199302000-00017.

Abstract

Recent studies have shown that MK801, a potent phencyclidine receptor ligand, causes pathomorphological changes in rat cerebrocortical neurones. Here we report that doses of MK801 (1 and 5 mg kg-1) which have been shown to produce pathomorphological changes, induce the expression of immediate-early gene proteins (IEGPs) and brain-derived neurotrophic factor (BDNF) mRNA in rat cerebrocortical neurones. Blockade of central muscarinic receptors which has been shown to prevent MK801-induced pathomorphological changes in cerebrocortical neurones, also prevented MK801-induced expression of IEGPs and BDNF mRNA. The transiently increased expression of BDNF mRNA may be an acute compensatory response of these neurones to MK801-induced injury.

摘要

近期研究表明,强效苯环利定受体配体MK801可引起大鼠大脑皮质神经元的病理形态学变化。在此我们报告,已证明能产生病理形态学变化的MK801剂量(1和5毫克/千克)可诱导大鼠大脑皮质神经元中即刻早期基因蛋白(IEGPs)的表达及脑源性神经营养因子(BDNF)mRNA的表达。已证明阻断中枢毒蕈碱受体可防止MK801诱导的大脑皮质神经元病理形态学变化,同时也可防止MK801诱导的IEGPs表达及BDNF mRNA表达。BDNF mRNA的短暂性表达增加可能是这些神经元对MK801诱导损伤的一种急性代偿反应。

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