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Background  Unlike mammals, zebrafish exhibits extensive neural regeneration after injury in adult stages of its lifetime due to the neurogenic activity of the radial glial cells. However, the genes involved in the regenerative neurogenesis response of the zebrafish brain are largely unknown. Thus, understanding the underlying principles of this regeneration capacity of the zebrafish brain is an interesting research realm that may offer vast clinical ramifications.    Results  In this paper, we characterized the expression pattern of  cxcr5  and analyzed the function of this gene during adult neurogenesis and regeneration of the zebrafish telencephalon. We found that  cxcr5  was upregulated transiently in the RGCs and neurons, and the expression in the immune cells such as leukocytes was negligible during both adult neurogenesis and regeneration. We observed that the transgenic misexpression of  cxcr5  in the ventricular cells using dominant negative and full-length variants of the gene resulted in altered proliferation and neurogenesis response of the RGCs. When we knocked down  cxcr5  using antisense morpholinos and cerebroventricular microinjection, we observed outcomes similar to the overexpression of the dominant negative  cxcr5  variant.    Conclusions  Thus, based on our results, we propose that  cxcr5  imposes a proliferative permissiveness to the radial glial cells and is required for differentiation of the RGCs to neurons, highlighting novel roles of  cxcr5  in the nervous system of vertebrates. We therefore suggest that  cxcr5  is an important cue for ventricular cell proliferation and regenerative neurogenesis in the adult zebrafish telencephalon. Further studies on the role of  cxcr5  in mediating neuronal replenishment have the potential to produce clinical ramifications in efforts for regenerative therapeutic applications for human neurological disorders or acute injuries.

The chemokine receptor cxcr5 regulates the regenerative neurogenesis response in the adult zebrafish brain