作者: Erzsebet Kovesdi , Andrea B. Gyorgy , Sook-Kyung C. Kwon , Daniel L. Wingo , Alaa Kamnaksh
关键词: Endocrinology 、 Psychology 、 Neurogenesis 、 Internal medicine 、 Traumatic brain injury 、 Hippocampal formation 、 Pathology 、 Environmental enrichment 、 Amygdala 、 Memory impairment 、 Hippocampus 、 Anxiety
摘要: De novo hippocampal neurogenesis contributes to functional recovery following traumatic brain injury (TBI). Enriched environment (EEN) can improve the outcome of TBI by positively affecting neurogenesis. Blast induced (bTBI) characterized memory impairment and increased anxiety levels, is a leading cause chronic disability among soldiers. Using rodent model bTBI we asked: a) whether long-term exposure EEN after ameliorate behavioral abnormalities b) what effects are at molecular cellular levels on de We found that housing injured animals in resulted significantly improved spatial while normal (NH) showed persistent impairment. VEGF Tau-protein but not IL-6 were normalized dorsal hippocampus (DHC) rats all three markers remained elevated NH rats. Interestingly, peaking 6 weeks post-injury, returned 2 months independent conditions. Housing had no significant effect ventral (VHC) amygdala (AD). also reduced INF VHC; these NH. observed an increase GFAP DCX immunoreactivities VHC post-injury. Conversely, housed or immunoreactivity their VHC. In summary, appears play positive role restoration functions anxiety, which period time. Cellular changes response appear be part neurogenesis-independent as well dependent processes triggered bTBI.