Ischemic brain damage in mice after selectively modifying BDNF or NT4 gene expression

Details

Serval ID
serval:BIB_056AB00B8D64
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Ischemic brain damage in mice after selectively modifying BDNF or NT4 gene expression
Journal
Journal of Cerebral Blood Flow and Metabolism
Author(s)
Endres  M., Fan  G., Hirt  L., Fujii  M., Matsushita  K., Liu  X., Jaenisch  R., Moskowitz  M. A.
ISSN
0271-678X (Print)
Publication state
Published
Issued date
01/2000
Peer-reviewed
Oui
Volume
20
Number
1
Pages
139-44
Notes
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. --- Old month value: Jan
Abstract
The neurotrophins and the tyrosine kinase (Trk) B receptor may play a protective role in the pathophysiology of cerebral ischemia. In this study, the authors investigated whether reducing endogenous expression of TrkB-binding neurotrophins modifies the susceptibility to ischemic injury after 1-hour middle cerebral artery occlusion followed by 23 hours of reperfusion in a filament middle cerebral artery occlusion model. Mice lacking both alleles for neurotrophin-4 (nt4-/-) or deficient in a single allele for brain-derived neurotrophic factor (bdnf+/-) exhibited larger cerebral infarcts compared to wild-type inbred 129/SVjae mice (68% and 91%, respectively, compared to controls). Moreover, lesions were larger (21%) in nt4-/- mice after permanent middle cerebral artery occlusion. Hence, expression of both NT4 and BDNF, and by inference the TrkB receptor, confers resistance to ischemic injury.
Keywords
Animals Arterial Occlusive Diseases/complications Brain Ischemia/*genetics/*pathology Brain-Derived Neurotrophic Factor/*genetics Cerebral Arteries Cerebral Cortex/metabolism Cerebral Infarction/etiology *Gene Expression Mice Mice, Knockout/genetics Nerve Growth Factors/*genetics RNA, Messenger/metabolism
Pubmed
Web of science
Create date
25/01/2008 12:40
Last modification date
20/08/2019 12:27
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