Hughes P, Dragunow M, Beilharz E, Lawlor P, Gluckman P
Department of Pharmacology, School of Medicine, University of Auckland, New Zealand.
Neuroreport. 1993 Feb;4(2):183-6. doi: 10.1097/00001756-199302000-00017.
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.
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。
