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Neurotrophin-3 promotes cell death induced in cerebral ischemia, oxygen-glucose deprivation, and oxidative stress: possible involvement of oxygen free radicals
Neurobiology of Disease
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. --- Old month value: Feb
To explore the role of neurotrophin-3 (NT-3) during cerebral ischemia, NT-3-deficient brains were subjected to transient focal ischemia. Conditional mutant brains produced undetectable amounts of NT-3 mRNA, whereas the expression of the neurotrophin, BDNF, the NT-3 receptor, TrkC, and the nonselective, low-affinity neurotrophin receptor p75NTR, were comparable to wild-type. Baseline absolute blood flow, vascular and neuroanatomical features, as well as physiological measurements were also indistinguishable from wild-type. Interestingly, the absence of NT-3 led to a significantly decreased infarct volume 23 h after middle cerebral artery occlusion. Consistent with this, the addition of NT-3 to primary cortical cell cultures exacerbated neuronal death caused by oxygen-glucose deprivation. Coincubation with the oxygen free radical chelator, trolox, diminished potentiation of neuronal death. NT-3 also enhanced neuronal cell death and the production of reactive oxygen species caused by oxidative damage inducing agents. We conclude that endogenous NT-3 enhanced neuronal injury during acute stroke, possible by increasing oxygen-radical mediated cell death.
Animals Brain/pathology Brain Chemistry/physiology Brain-Derived Neurotrophic Factor/genetics Cell Death/*physiology Cells, Cultured Free Radicals/metabolism Glucose/metabolism Ischemic Attack, Transient/*metabolism/pathology Mice Mice, Neurologic Mutants Neurons/cytology Neurotrophin 3/*genetics/*metabolism Oxidative Stress/physiology Oxygen/metabolism RNA, Messenger/analysis Reactive Oxygen Species/metabolism Receptor, Nerve Growth Factor/genetics Receptor, trkC/genetics
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