Brain-derived neurotrophic factor reduces cortical cell death by ischemia after middle cerebral artery occlusion in the rat.

摘要: Stroke is the major cause of adult brain dysfunction. In an experimental approach to evaluate possible beneficial effects administration neurotrophic factors in stroke, we have used a model distal middle cerebral artery (MCA) occlusion rats. this model, found: (1) permanent reduction brain-derived factor (BDNF) and its full-length receptor, TrkB, infarcted core; (2) transient increase BDNF immunoreactivity internal region border infarct (penumbra area) at 12 h after MCA occlusion; (3) increased truncated TrkB astrocytes surrounding area infarction; (4) scattered neurons, distant from infarct, ipsilateral contralateral cortices 24 48 occlusion. We next studied regulation expression by BDNF, ischemia, neuroprotective vivo. control non-ischemic rats, grafting mock- or BDNF-transfected fibroblasts (F3A-MT F3N-BDNF cell lines, respectively) medial part somatosensory cortex neighboring astrocytes. Grafting alone also vicinity mock graft (at h) BDNF-grafted 4 days). Interestingly, ischemic animals grafted with mock-transfected line did not show any further receptors. However, showed up-regulation neurons located infarct. Analysis nuclear DNA fragmentation situ, combined microtubule-associated protein 2 immunohistochemistry, revealed that most cells dying borders following were neurons. No differences size found between occluded, MCA-occluded, MCA-occluded Moreover, death was similar nongrafted mock-grafted rats subjected number breaks significantly reduced penumbra close Thus, our results specifically up-regulates receptor cortical prevents their vivo focal ischemia.