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伊博格碱引起的兴奋性毒性损伤导致浦肯野细胞中神经元型一氧化氮合酶的延迟诱导。

Excitotoxic insult due to ibogaine leads to delayed induction of neuronal NOS in Purkinje cells.

作者信息

O'Hearn E, Zhang P, Molliver M E

机构信息

Department of Neurology and Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185, USA.

出版信息

Neuroreport. 1995 Aug 21;6(12):1611-6. doi: 10.1097/00001756-199508000-00006.

Abstract

Ibogaine causes degeneration of Purkinje cells (PKCs), presumably via activation of neurons in the inferior olive leading to release of glutamate at climbing fiber terminals. Following ibogaine administration, some Purkinje cells express NADPH-diaphorase and neuronal NOS (nNOS), neither of which is present normally in these cells. The induction of NOS is delayed in onset, dose-related, and detected in neurons adjacent to degenerated PKCs. The results demonstrate that nNOS induction can follow excitotoxic neuronal injury or perturbation. However, NO is unlikely to participate in the initial phase of PKC damage. Both the late induction of nNOS and the spatial relationship between damaged and nNOS-expressing PKCs are consistent with a role for NO in either neuronal recovery or delayed cell death following excitotoxic injury.

摘要

伊博格碱可导致浦肯野细胞(PKCs)变性,推测是通过激活下橄榄核中的神经元,导致攀爬纤维终末释放谷氨酸。给予伊博格碱后,一些浦肯野细胞表达烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPH-d)和神经元型一氧化氮合酶(nNOS),而这些细胞正常情况下均不表达。一氧化氮合酶的诱导在开始时延迟,与剂量相关,并在变性浦肯野细胞相邻的神经元中检测到。结果表明,nNOS的诱导可发生在兴奋性毒性神经元损伤或干扰之后。然而,一氧化氮不太可能参与浦肯野细胞损伤的初始阶段。nNOS的延迟诱导以及受损的和表达nNOS的浦肯野细胞之间的空间关系均表明,一氧化氮在兴奋性毒性损伤后的神经元恢复或延迟细胞死亡中发挥作用。

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