Article: article from journal or magazin.
Ischemic brain damage in mice after selectively modifying BDNF or NT4 gene expression
Journal of Cerebral Blood Flow and Metabolism
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. --- Old month value: Jan
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.
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
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