Progeny of Olig2-Expressing Progenitors in the Gray and White Matter of the Adult Mouse Cerebral Cortex

Abstract

Despite their abundance, still little is known about the rather frequent, constantly proliferating progenitors spread throughout the adult mouse brain parenchyma. The majority of these progenitors express the basic-helix-loop-helix transcription factor Olig2, and their number further increases after injury. Here, we examine the progeny of this progenitor population by genetic fate mapping using tamoxifen-inducible Cre-recombination in the Olig2 locus to turn on permanent reporter gene expression in the adult brain. Consistent with Olig2 expression in proliferating NG2 ϩ progenitors, most reporter ϩ cells seen shortly after initiating recombination at adult stages incorporated BrdU and contained the proteoglycan NG2 in both the gray (GM) and the white matter (WM) of the cerebral cortex. However, at longer time points after induction, we observed profound differences in the identity of reporter ϩ cells in the WM and GM. Whereas most of the Olig2 ϩ progenitors had generated mature, myelinating oligodendrocytes in the WM, hardly any reporter ϩ cells showing mature oligodendrocyte characteristics were detectable even up to 6 months after recombination in the GM. In the GM, most reporter ϩ cells remained NG2 ϩ , even after injury, but stopped proliferating rather soon after recombination. Thus, our results demonstrate the continuous generation of mature, myelinating oligodendrocytes in the WM, whereas cells in the GM generated mostly postmitotic NG2 ϩ glia.

A new role for the P2Y-like GPR17 receptor in the modulation of multipotency of oligodendrocyte precursor cells in vitro

“…For example, following brain ischemia due to permanent middle cerebral artery occlusion (MCAo), generation of both astrocytic and neuronal precursors from NG2 + cells was observed in adult NG2creBAC:ZEG double transgenic mice, in which enhanced green fluorescent protein (EGFP) is expressed in OPCs and their progeny, thus allowing to visualize their final phenotype [10]. However, conflicting data arise from the different transgenic mouse models employed, and the controversy around the multipotency and neurogenic potential of OPCs in vivo is still an open issue [11][12][13][14][15].…”

Sonic Hedgehog Pathway Activation Is Induced by Acute Brain Injury and Regulated by Injury-Related Inflammation

“…ϩ precursors appear to have the highest capacity for proliferation in vivo after brain injury (Zaidi et al, 2004;Buffo et al, 2005;Dimou et al, 2008).…”

Expression of the transcription factor Olig2 in proliferating cells in the adult zebrafish telencephalon

“…Interestingly, the mouse cortex contains also a large fraction of oligodendrocyte precursors cells that are tightly associated with neurons and do not synthesize Mbp (Trotter et al, 2010). Fate-mapping studies in the mouse showed that although these cells are mostly quiescent, they can be activated to divide and can give rise to oligodendrocytes, to neurons in the piriform cortex, and also to astrocytes (Kim et al, 2007;Dimou et al, 2008;Rivers et al, 2008;Zhao et al, 2009). These cells, which have processes that contact neurons, were variably referred to as polydendrocytes or more generally as OPCs in the mouse and rat (Wolswijk and Noble, 1989;Nishiyama et al, 1999Nishiyama et al, , 2009Hermann et al, 2010).…”