Fig. 1. CNTF/LIF/gp130 receptor signaling promotes the self-renewal/expansion of FGF-responsive neural stem cells (NSCs) from the ventricular zone (VZ) of the ventral forebrain. E9.5 ventral neuroepithelial cells expressed the FGF receptors FGFR1 (A) and FGFR2 (B). CNTFR expression (C) was not observed; however, LIFRß (D) was expressed. At E11.5, FGFR1 (E), FGFR2 (F), CNTFR (G) and LIFRß (H) were expressed within the LGE VZ. Double-labeling of the E14.5 LGE for FGFR2 (I) and Ki67 (J), as well as LIFRß (K) and Ki67 (L), revealed receptor expression by VZ precursors, not SVZ precursors (arrows in J,L indicate examples of co-expressing cells). (M) The total number of cells generated in pass 1 FGF-2 neurosphere cultures doubled in the presence of either CNTF (F+C) (^**P=0.009; n=5) or LIF (F+L) (^*P=0.026; n=5). (N) The total number of neurospheres generated in pass 1 FGF-2 neurosphere cultures was not changed by the addition of either CNTF or LIF (n=3). (O,P) The number of neurospheres that were 200 µm or greater in diameter was doubled by the addition of either CNTF (^**P=0.0003) or LIF (^**P=0.005; results are normalized to FGF control; n=3). (Q) CNTF (^*P=0.03) and LIF (^*P=0.04) significantly increased the percentage of cells that expressed the undifferentiated cell marker nestin in pass 1 FGF2 neurosphere cultures (n=3). (R) The number of secondary neurospheres formed in FGF-2 alone per 2000 cells plated was significantly increased by either CNTF (^*P=0.02) or LIF (^*P=0.02; results are normalized to FGF control; n=3). Scale bars: in A, 50 µm for A-H; in I, 50 µm (25 µm in enlarged images) for I-L; in O, 100 µm.