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兴奋性毒性在青光眼发病机制中的可能作用。

Possible role of excitotoxicity in the pathogenesis of glaucoma.

作者信息

Casson Robert J

机构信息

Department of Ophthalmology and Visual Science, Royal Adelaide Hospital, North Tce., Adelaide, SA 5000, Australia.

出版信息

Clin Exp Ophthalmol. 2006 Jan-Feb;34(1):54-63. doi: 10.1111/j.1442-9071.2006.01146.x.

Abstract

Excitotoxicity describes the process of neuronal injury by excess stimulation of amino acid receptors. This form of insult was first described in the retina, and subsequently has been shown to be an important component of the pathogenesis of ischaemic and traumatic injury in the central nervous system. Furthermore, there is increasing evidence that excitotoxicity is involved in several chronic neurological conditions, and anti-excitotoxic treatment has already been approved for some of these conditions. A large-scale trial is currently underway that will determine the efficacy of an anti-excitotoxic drug (memantine) in the management of glaucoma. This review provides an overview of neurotransmission and the mechanisms of excitotoxicity. The evidence for excitotoxicity as a component of certain neurological diseases, including glaucoma, is discussed.

摘要

兴奋性毒性描述了因氨基酸受体过度刺激而导致神经元损伤的过程。这种损伤形式最初在视网膜中被描述,随后被证明是中枢神经系统缺血性和创伤性损伤发病机制的重要组成部分。此外,越来越多的证据表明兴奋性毒性与几种慢性神经疾病有关,并且针对其中一些疾病的抗兴奋性毒性治疗已获批准。目前正在进行一项大规模试验,以确定一种抗兴奋性毒性药物(美金刚)在青光眼治疗中的疗效。本综述概述了神经传递和兴奋性毒性的机制。文中讨论了兴奋性毒性作为某些神经疾病(包括青光眼)的一个组成部分的证据。

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