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Fig. 2. Retinoid signaling increases neurogenesis in P15 mouse SVZ NS cultures. (A)
RA treatment of differentiating NS for 7 DIV increases the percentage of
neurons and decreases that of astrocytes in a concentration-dependent manner;
**P<0.0001 versus vehicle or 0.2 µM RA groups;
*P<0.001 versus vehicle or 0.2 µM RA groups.
Oligodendrocyte differentiation is unchanged by RA exposure. (B) RA (1 µM)
or retinol (Ret; 1 µM) treatment increases differentiating neurons after 7
DIV versus vehicle (Veh); the addition of disulfiram (DS) inhibits the retinol
effect. *P< 0.0001 versus Veh or Ret/DS; +,
P<0.001 versus Ret; #P<0.0005 versus Veh or Ret/DS.
(C,D) At 4 DIV, 1 µM RA increases the proportion of proliferating
neuroblasts (BrdU/ß-tubulin double-labeled) compared with total or
BrdU-positive cells, and decreases the proportion of BrdU/GFAP double-labeled
astrocytes. The proportion (%) of cells incorporating BrdU also significantly
increases after RA exposure (C). For C and D, *denotes
P<0.05 and **denotes P<0.005. (E) RA does
not influence numbers of activated caspase-3-immunoreactive (dying) cells.
(F,G) Secondary NS cultures were treated with vehicle (A) or 1 µM RA (B)
for 6 days in expansion conditions. RA-treated NS are smaller and appear more
differentiated with irregular morphology and process outgrowth (arrows). (H,I)
When RA- or vehicle-treated secondary NS were passaged and expanded without
RA, the tertiary NS not previously exposed to RA were larger and more numerous
(H) compared with those treated with RA before passaging (I). Scale bar: 50
µm.
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