Background and ObjectiveAccumulating evidence has shown that low-power laser irradiation (LLI) affects cell proliferation and survival, but little is known about LLI effects on neural stem/progenitor cells (NSPCs). Here we investigate whether transcranial 532 nm LLI affects NSPCs in adult murine neocortex and in neurospheres from embryonic mice.Study Design/Materials and MethodsWe applied 532 nm LLI (Nd:YVO4, CW, 60 mW) on neocortical surface via cranium in adult mice and on cultured cells from embryonic mouse brains in vitro to investigate the proliferation and migration of NSPCs and Akt expression using immunohistochemical assays and Western blotting techniques.ResultsIn vivo experiments demonstrated that 532 nm LLI significantly facilitated the migration of GABAergic NSPCs that were induced to proliferate in layer 1 by mild ischemia. In vitro experiments using GABAergic NSPCs derived from embryonic day 14 ganglionic eminence demonstrated that 532 nm LLI for 60 min promoted the migration of GAD67-immunopositive NSPCs with a significant increase of Akt expression. Meanwhile, the LLI induced proliferation, but not migration, of NSPCs that give rise to excitatory neurons.ConclusionIt is concluded that 532 nm LLI promoted the migration of GABAergic NSPCs into deeper layers of the neocortex in vivo by elevating Akt expression.

Sensory experience influences proliferation and differentiation of oligodendrocyte progenitor cells (OPCs). Enhanced sensorimotor experience promoted the lineage progression of OPCs and myelination in the gray matter and white matter (WM) of sensorimotor cortex. In the visual cortex, reduced experience reportedly delayed the maturation of myelination in the gray matter, but whether and how such experience alters the subcortical WM is unclear. Here we investigated if binocular enucleation from the onset of eye opening (i.e., P15) affects the cell state of OPCs in mouse primary visual cortex (V1). Proliferative cells in the WM declined nearly half over 3 days from postnatal day (P) 25. A 3-day BrdU-labeling showed gradual decline in proliferation rates from P19 to P28. Binocular enucleation resulted in an increase in the cycling state of the OPCs that were proliferated from P22 to P25 but not before or after this period. This increase in proliferative OPCs was not associated with lineage progression toward differentiated oligodendrocytes. Proliferative OPCs arose mostly due to symmetric cell division but also asymmetric formation of proliferative and quiescent OPCs. By P30, almost all the proliferated cells exited the cell cycle. Maturing oligodendrocytes among the proliferated cells increased at this age, but most of them disappeared over 25 days. The cell density of the maturing oligodendrocytes was unaffected by binocular enucleation, however. These data suggest that binocular enucleation transiently elevates proliferative OPCs in the subcortical WM of V1 during a specific period of the fourth postnatal week without subsequently affecting the number of maturing oligodendrocytes several days later.

Sensory experience modulates proliferation, differentiation, and migration of oligodendrocyte progenitor cells (OPCs). In the mouse primary visual cortex (V1), visual deprivation-dependent modulation of OPCs has not been demonstrated. Here, we demonstrate that undifferentiated OPCs developmentally peaked around postnatal day (P) 25, and binocular enucleation (BE) from the time of eye opening (P14-15) elevated symmetrically-divided undifferentiated OPCs in a reversible G0/G1 state even more at the bottom lamina of the cortex by reducing maturing oligodendrocyte (OL) lineage cells. Experiments using the sonic hedgehog (Shh) signaling inhibitor cyclopamine in vivo suggested that Shh signaling pathway was involved in the BE-induced undifferentiation process. The undifferentiated OPCs then differentiated within 5 days, independent of the experience, becoming mostly quiescent cells in control mice, while altering the mode of sister cell symmetry and forming quiescent as well as maturing cells in the enucleated mice. At P50, BE increased mature OLs via symmetric and asymmetric modes of cell segregation, resulting in more populated mature OLs at the bottom layer of the cortex. These data suggest that fourth postnatal week, corresponding to the early critical period of ocular dominance plasticity, is a developmentally sensitive period for OPC state changes. Overall, the visual loss promoted undifferentiation at the early period, but later increased the formation of mature OLs via a change in the mode of cell type symmetry at the bottom layer of mouse V1.