狂犬病病毒对原代神经元培养物和成年小鼠的感染：未能证明存在兴奋性毒性的证据。
Rabies virus infection of primary neuronal cultures and adult mice: failure to demonstrate evidence of excitotoxicity.
作者信息
Weli Simon C, Scott Courtney A, Ward Christopher A, Jackson Alan C
机构信息
Kingston General Hospital, 76 Stuart Street, Connell 725, Kingston, ON, Canada K7L 2V7.
出版信息
J Virol. 2006 Oct;80(20):10270-3. doi: 10.1128/JVI.01272-06.
Abstract
Cultures derived from the cerebral cortices and hippocampi of 17-day-old mouse fetuses infected with the CVS strain of rabies virus showed loss of trypan blue exclusion, morphological apoptotic features, and activated caspase 3 expression, indicating apoptosis. The NMDA (N-methyl-D-aspartate acid) antagonists ketamine (125 microM) and MK-801 (60 microM) were found to have no significant neuroprotective effect on CVS-infected neurons, while the caspase inhibitor Ac-Asp-Glu-Val aspartic acid aldehyde (25 microM) exerted a marked neuroprotective effect. Glutamate-stimulated increases in levels of intracellular calcium were reduced in CVS-infected hippocampal neurons. Ketamine (120 mg/kg of body weight/day intraperitoneally) given to CVS-infected adult mice produced no beneficial effects. We have found no supportive evidence that excitotoxicity plays an important role in rabies virus infection.
摘要
从感染狂犬病病毒CVS株的17日龄小鼠胎儿的大脑皮质和海马体中获得的培养物显示，锥虫蓝排斥丧失、形态学凋亡特征以及活化的半胱天冬酶3表达，表明存在凋亡。发现NMDA（N-甲基-D-天冬氨酸）拮抗剂氯胺酮（125微摩尔）和MK-801（60微摩尔）对感染CVS的神经元没有显著的神经保护作用，而半胱天冬酶抑制剂Ac-Asp-Glu-Val天冬氨酸醛（25微摩尔）发挥了显著的神经保护作用。在感染CVS的海马神经元中，谷氨酸刺激引起的细胞内钙水平升高有所降低。给感染CVS的成年小鼠腹腔注射氯胺酮（120毫克/千克体重/天）没有产生有益效果。我们没有发现支持兴奋性毒性在狂犬病病毒感染中起重要作用的证据。
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