Training of the impaired forelimb after traumatic brain injury enhances hippocampal neurogenesis in the Emx1 null mice lacking a corpus callosum.

摘要: Unilateral brain injury is known to disrupt the balance between two cortices, as evidenced by an abnormally high interhemispheric inhibitory drive from motor cortex M1intact M1lesioned transmitted transcallosally. Our previous work has shown that deletion of homeobox gene Emx1 not only led agenesis corpus callosum (cc), but also reduced hippocampal neurogenesis. The current study sought determine whether lacking cc affected recovery forelimb function and plasticity following training limb in mice with unilateral traumatic injuries (TBI). One week after TBI, produced a controlled cortical impact impair preferred limb, wild type (WT) knock out (KO) were subjected single-pellet reaching task for 4 weeks. Both TBI had overall adverse effects on successful rate reaching. However, significantly performance WT KO mice. negatively neurogenesis, demonstrated reduction doublecortin (DCX)-expressing immature neurons, while enhanced DCX expression. increased cells TBI-treated group, whereas it induced neurogenesis both groups regardless treatment. finding suggests enhances neuroplasticity at functionally remote regions including hippocampus, which may have implications promoting TBI.