视神经轴突缺血性损伤的基本原理。

R Fern, B R Ransom
{"title":"视神经轴突缺血性损伤的基本原理。","authors":"R Fern,&nbsp;B R Ransom","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Anterior ischemic optic neuropathy is the most common cause of persistent monocular visual loss in persons over the age of 50. At the heart of this form of optic neuropathy is a sequence of cytoplasmic and membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these events. Preventing or modulating any of these well-defined steps mitigates against the development of anoxic injury. Translating these molecular insights about how optic nerve axons are damaged by ischemia-like conditions into clinical gains remains the challenge for the future.</p>","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"4 5","pages":"246-50"},"PeriodicalIF":0.0000,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ischemic injury of optic nerve axons: the nuts and bolts.\",\"authors\":\"R Fern,&nbsp;B R Ransom\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Anterior ischemic optic neuropathy is the most common cause of persistent monocular visual loss in persons over the age of 50. At the heart of this form of optic neuropathy is a sequence of cytoplasmic and membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these events. Preventing or modulating any of these well-defined steps mitigates against the development of anoxic injury. Translating these molecular insights about how optic nerve axons are damaged by ischemia-like conditions into clinical gains remains the challenge for the future.</p>\",\"PeriodicalId\":79395,\"journal\":{\"name\":\"Clinical neuroscience (New York, N.Y.)\",\"volume\":\"4 5\",\"pages\":\"246-50\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1997-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical neuroscience (New York, N.Y.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical neuroscience (New York, N.Y.)","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

前部缺血性视神经病变是50岁以上人群持续性单眼视力丧失的最常见原因。这种视神经病变的核心是一系列细胞质和膜事件,最终导致轴突破坏。ATP的早期耗竭随后是膜去极化,Na+和Ca2+通过特定的电压门控通道内流,以及Na+/Ca2+交换蛋白的反向操作。有毒Ca2+超载是这些事件的最终后果。预防或调节任何这些明确的步骤减轻对缺氧损伤的发展。将这些关于视神经轴突如何被缺血样条件损伤的分子见解转化为临床成果仍然是未来的挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ischemic injury of optic nerve axons: the nuts and bolts.

Anterior ischemic optic neuropathy is the most common cause of persistent monocular visual loss in persons over the age of 50. At the heart of this form of optic neuropathy is a sequence of cytoplasmic and membrane events that culminate in axonal destruction. Early depletion of ATP is followed by membrane depolarization, influx of Na+ and Ca2+ via specific voltage-gated channels and reverse operation of the Na+/Ca2+ exchange protein. Toxic Ca2+ overload is the ultimate consequence of these events. Preventing or modulating any of these well-defined steps mitigates against the development of anoxic injury. Translating these molecular insights about how optic nerve axons are damaged by ischemia-like conditions into clinical gains remains the challenge for the future.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信