Conditional Depletion of Neurogenesis Inhibits Long-Term Recovery after Experimental Stroke in MiceReportar como inadecuado




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We reported previously that ablation of doublecortin DCX-immunopositive newborn neurons in mice worsens anatomical and functional outcome measured 1 day after experimental stroke, but whether this effect persists is unknown. We generated transgenic mice that express herpes simplex virus thymidine kinase under control of the DCX promoter DCX-TK transgenic mice. DCX-expressing and recently divided cells in the rostral subventricular zone SVZ and hippocampus of DCX-TK transgenic mice, but not wild-type mice, were specifically depleted after ganciclovir GCV treatment for 14 days. Focal cerebral ischemia was induced by permanent distal middle cerebral artery occlusion MCAO on day 14 of vehicle or GCV treatment, and mice were killed 12 weeks after MCAO. Infarct volume was significantly increased and neurologic deficits were more severe in GCV- compared to vehicle-treated DCX-TK transgenic mice at first 8 weeks, after depletion of DCX- and bromodeoxyuridine-immunoreactive cells in the SVZ and dentate gyrus following focal ischemia. Our results indicate that endogenous neurogenesis in a critical period following experimental stroke influences the course of long-term recovery.



Autor: Xiaomei Wang, XiaoOu Mao, Lin Xie, Fen Sun, David A. Greenberg, Kunlin Jin

Fuente: http://plos.srce.hr/



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