Jackson A C
Department of Medicine, Queen's University, Kingston, Ontario, Canada.
Acta Virol. 1993 Dec;37(6):502-8.
A defect in cholinergic synaptic neurotransmission could explain the neuronal dysfunction that has been observed in rabies. The enzymatic activities of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and enolase were assessed in the brains of rabies virus strain CVS-infected and uninfected mice. No statistically significant differences in activities of ChAT, AChE, or enolase were observed in the cerebral cortex or hippocampus of moribund CVS-infected mice versus controls. Binding to muscarinic acetylcholine receptors, which was assessed with 3H-labelled quinuclidinyl benzylate (QNB), was also not significantly different in the cerebral cortex or hippocampus of CVS-infected mice and uninfected controls. The studies suggest that dysfunction of the cholinergic system is unlikely of fundamental importance in this mouse model of rabies.
胆碱能突触神经传递缺陷可能解释狂犬病中观察到的神经元功能障碍。在狂犬病病毒株CVS感染和未感染的小鼠大脑中评估了胆碱乙酰转移酶(ChAT)、乙酰胆碱酯酶(AChE)和烯醇化酶的酶活性。与对照组相比,濒死的CVS感染小鼠的大脑皮层或海马中ChAT、AChE或烯醇化酶的活性没有统计学上的显著差异。用3H标记的喹核苄酯(QNB)评估的与毒蕈碱型乙酰胆碱受体的结合,在CVS感染小鼠和未感染对照的大脑皮层或海马中也没有显著差异。这些研究表明,在这个狂犬病小鼠模型中,胆碱能系统功能障碍不太可能具有根本重要性。