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

First Author  Endres M Year  2000
Journal  J Cereb Blood Flow Metab Volume  20
Issue  1 Pages  139-44
PubMed ID  10616802 Mgi Jnum  J:60087
Mgi Id  MGI:1352609 Doi  10.1097/00004647-200001000-00018
Citation  Endres M, et al. (2000) Ischemic brain damage in mice after selectively modifying BDNF or NT4 gene expression. J Cereb Blood Flow Metab 20(1):139-44
abstractText  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.
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