Source:http://linkedlifedata.com/resource/pubmed/id/17494711
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
19
|
| pubmed:dateCreated |
2007-5-14
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| pubmed:abstractText |
Transient forebrain ischemia induces delayed, selective neuronal death in the CA1 region of the hippocampus. The underlying molecular mechanisms are as yet unclear, but it is known that activation of L-type Ca2+ channels specifically increases the expression of a group of genes required for neuronal survival. Accordingly, we examined temporal changes in L-type calcium-channel activity in CA1 and CA3 pyramidal neurons of rat hippocampus after transient forebrain ischemia by patch-clamp techniques. In vulnerable CA1 neurons, L-type Ca2+-channel activity was persistently downregulated after ischemic insult, whereas in invulnerable CA3 neurons, no change occurred. Downregulation of L-type calcium channels was partially caused by oxidation modulation in postischemic channels. Furthermore, L-type but neither N-type nor P/Q-type Ca2+-channel antagonists alone significantly inhibited the survival of cultured hippocampal neurons. In contrast, specific L-type calcium-channel agonist remarkably reduced neuronal cell death and restored the inhibited channels induced by nitric oxide donor. More importantly, L-type calcium-channel agonist applied after reoxygenation or reperfusion significantly decreased neuronal injury in in vitro oxygen-glucose deprivation ischemic model and in animals subjected to forebrain ischemia-reperfusion. Together, the present results suggest that ischemia-induced inhibition of L-type calcium currents may give rise to delayed death of neurons in the CA1 region, possibly via oxidation mechanisms. Our findings may lead to a new perspective on neuronal death after ischemic insult and suggest that a novel therapeutic approach, activation of L-type calcium channels, could be tested at late stages of reperfusion for stroke treatment.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
1529-2401
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| pubmed:author |
pubmed-author:GaoTian-MingTM,
pubmed-author:HouFeng-QingFQ,
pubmed-author:HuDe-HuiDH,
pubmed-author:HuPingP,
pubmed-author:LiJian-GuoJG,
pubmed-author:LiXiao-MingXM,
pubmed-author:LiangChenC,
pubmed-author:QinLu-NingLN,
pubmed-author:WangYingY,
pubmed-author:YangJian-MingJM,
pubmed-author:ZhaoMiaoM,
pubmed-author:ZhuXin-HongXH
|
| pubmed:issnType |
Electronic
|
| pubmed:day |
9
|
| pubmed:volume |
27
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
5249-59
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| pubmed:meshHeading |
pubmed-meshheading:17494711-Animals,
pubmed-meshheading:17494711-Brain Infarction,
pubmed-meshheading:17494711-Brain Ischemia,
pubmed-meshheading:17494711-Calcium Channel Agonists,
pubmed-meshheading:17494711-Calcium Channel Blockers,
pubmed-meshheading:17494711-Calcium Channels, L-Type,
pubmed-meshheading:17494711-Calcium Signaling,
pubmed-meshheading:17494711-Cell Death,
pubmed-meshheading:17494711-Cell Survival,
pubmed-meshheading:17494711-Down-Regulation,
pubmed-meshheading:17494711-Hippocampus,
pubmed-meshheading:17494711-Male,
pubmed-meshheading:17494711-Nerve Degeneration,
pubmed-meshheading:17494711-Neurons,
pubmed-meshheading:17494711-Organ Culture Techniques,
pubmed-meshheading:17494711-Oxidative Stress,
pubmed-meshheading:17494711-Patch-Clamp Techniques,
pubmed-meshheading:17494711-Pyramidal Cells,
pubmed-meshheading:17494711-Rats,
pubmed-meshheading:17494711-Rats, Wistar,
pubmed-meshheading:17494711-Reperfusion Injury,
pubmed-meshheading:17494711-Time Factors
|
| pubmed:year |
2007
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| pubmed:articleTitle |
Contribution of downregulation of L-type calcium currents to delayed neuronal death in rat hippocampus after global cerebral ischemia and reperfusion.
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| pubmed:affiliation |
Department of Anatomy and Neurobiology, Southern Medical University, Guangzhou 510515, People's Republic of China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|