期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 37, 期 -, 页码 1147-1160出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0371147
关键词
calcium signalling; neurodegeneration; neuroprotection; N-methyl-D-aspartate receptor (NMDAR); oxidative stress; transcription
资金
- Royal Society
- Wellcome Trust
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- European Commission
- Medical Research Scotland
- European Molecular Biology Organization Young Investigator Programme
- Biotechnology and Biological Sciences Research Council [BB/D011388/1] Funding Source: researchfish
- BBSRC [BB/D011388/1] Funding Source: UKRI
NMDA (N-methyl-D-aspartate) receptors are a subtype of ionotropic glutamate receptor with an important role in the physiology and pathophysiology of central neurons. inappropriate levels of Ca2+ influx through the NMDA receptor can contribute to neuronal loss in acute trauma such as ischaemia and traumatic brain injury, as well as certain neurodegenerative diseases such as Huntington's disease. However, normal physiological patterns of NMDA receptor activity can promote neuroprotection against both apoptotic and excitotoxic insults. As a result, NMDA receptor blockade can promote neuronal death outright or render neurons vulnerable to secondary trauma. Thus responses to NMDA receptor activity follow a classical hormetic dose-response curve: both too much and too little can be harmful. There is a growing knowledge of the molecular mechanisms underlying both the neuroprotective and neurodestructive effects of NMCA receptor activity, as well as the factors that determine whether an episode of NMCA receptor activity is harmful or beneficial. it is becoming apparent that oxidative stress plays a role in promoting neuronal death in response to both hyper- and hypo-activity of the NMDA receptor. increased understanding in this field is leading to the discovery of new therapeutic targets and strategies for excitotoxic disorders, as well as a growing appreciation of the harmful consequences of NMDA receptor blockade.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据