It was highly expressed in the hypoglossal, trigeminal motor and sensory, cochlear. It had been also expressed in the pontine reticular nucleus and reticular section of substantia nigra. These observations show that, like BAI1 and BAI2, BAI3 can be a neuron particular protein, and that the localization of BAI3 expression in the head coincides with that of BAI1 or BAI2. To verify the Northern information the neonatal brain has higher degrees of BAI3 expression compared to the person, in-situ hybridization experiment was done to the neonatal cerebral cortex of 2, 3 and 8 weeks old brain. At 14 days, a high activity of the BAI3 was recognized throughout the whole cerebral cortex. BAI3 decreased slightly in the entire cerebral order FK228 cortex at 3 weeks, but decreased generally speaking at 8 weeks. Nevertheless, it showed a powerful hybridization signal generally in most neurons of levels II III at 8 weeks. These results show that BAI3 was highly expressed in neonatal brain, and it was derived from neuron specific expression, although not from caused by glial expression of BAI3. The temporal expression profiles of BAI3 and VEGF in ischemic cerebral tissues were calculated in the in vivo focal cerebral ischemia model, to analyze the role of BAI3 in ischemia induced brain angiogenesis. Western blot analyses of the ischemic part Chromoblastomycosis of the cerebral cortex using specific anti-bodies acknowledged 170 and 2-5 kDa groups equivalent to VEGF and BAI3 proteins, respectively. The expression of BAI3 reduced around the part of-the brain at 0. 5 h after ischemia until 8 h, in contrast to sham operated cerebral cortex, but it slowly recovered by 24 h. BAI3 level was significantly reduced through-out all experimental periods compared with that of control. The amount of VEGF expression was transiently increased in-the ischemic cortex at 0. 5 h, peaked at 8 h, and it returned to basal level at 24 h after ischemia. VEGF level was notably increased at 8 h in contrast to that of control. The ischemic mind may possibly stimulate angiogenesis to compensate for impaired blood circulation. TSP1 and TSP2 are naturally-occurring angiostatic facets that inhibit angiogenesis in vivo and in-vitro. The roles of BAIs and TSP within the regulation of postischemic angiogenesis aren’t completely known. Recently, we documented that angiostatic BAI2 enjoyed in ischemiainduced mind angiogenesis in concert with angiogenic MAPK assay VEGF. The expression of BAI2 decreased in the ischemic part of cerebral cortex after 1 h in contrast to sham operated one and the decreased level was maintained at 2 h, but was slowly recovered after 8 h. Although, VEGF reached its peak level within the ischemic cerebral cortex and contralateral non ischemic one after 8 h, but was returned to manage level at 24 h.