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• W2497041907 abstract "Despite the presence of on-going neurogenesis in the adult mammalian brain, neurons are generally not replaced after injury. Using a rodent model of excitotoxic cell loss and retroviral (RV) lineage tracing, we previously demonstrated transient recruitment of precursor cells from the subventricular zone (SVZ) into the lesioned striatum. In the current study we determined that these cells included migratory neuroblasts and oligodendrocyte precursor cells (OPC), with the predominant response from glial cells. We attempted to override this glial response by ectopic expression of the pro-neurogenic genes Pax6 or Dlx2 in the adult rat SVZ following quinolinic acid lesioning. RV-Dlx2 over-expression stimulated repair at a previously non-neurogenic time point by enhancing neuroblast recruitment and the percentage of cells that retained a neuronal fate within the lesioned area, compared to RV-GFP controls. RV-Pax6 expression was unsuccessful at inhibiting glial fate and intriguingly, increased OPC cell numbers with no change in neuronal recruitment. These findings suggest that gene choice is important when attempting to augment endogenous repair as the lesioned environment can overcome pro-neurogenic gene expression. Dlx2 over-expression however was able to partially overcome an anti-neuronal environment and therefore is a promising candidate for further study of striatal regeneration." @default.
• W2497041907 created "2016-08-23" @default.
• W2497041907 creator A5031490344 @default.
• W2497041907 creator A5061103470 @default.
• W2497041907 date "2016-05-30" @default.
• W2497041907 modified "2023-09-28" @default.
• W2497041907 title "The Effect of Pro-Neurogenic Gene Expression on Adult Subventricular Zone Precursor Cell Recruitment and Fate Determination After Excitotoxic Brain Injury" @default.
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• W2497041907 doi "https://doi.org/10.46582/jsrm.1201005" @default.
• W2497041907 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4929891" @default.
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• W2497041907 hasPublicationYear "2016" @default.
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