Figure 7. Cholinergic differentiation is impaired in p38β-deficient neurons in vitro and in vivo. A, Representative photograph of mouse SCGs at postnatal day 6 from either wild-type (WT) or p38β-deficient mice. B, Images of primary mouse SCG neurons from WT and p38β−/− mice 48 h after plating in the presence of CNTF and NGF. No differences in cell morphology, neurite outgrowth, or cell number was observed depending on the genotype (scale bar, 20 μm). C, Representative Western blot and quantified results showing a significant increase in p38 phosphorylation in CNTF-treated mouse SCG neurons in comparison to NGF-treated cultures. Tubulin was used as a loading control (n = 3). D, 38β deficiency in CNTF-treated mouse SCG neurons greatly reduces Chat, Vacht, and VIP transcript levels, without affecting Net, Tau, and p38α levels in comparison with CNTF-treated wild-type cultures after 48 h in culture (n = 4). E, Sections from postnatal day 60 mouse stellate ganglia were immunostained for Vacht in wild-type and p38β−/− mice. Vacht-positive cell somata are indicated by white arrows (scale bar 20 μm). Quantitative analysis of Vacht-immunoreactive neurons per ganglion demonstrates that the number of Vacht-positive cells is greatly reduced in p38β mutant ganglia. The percentage of Vacht-IR neurons per ganglion was calculated as Vacht/DAPI-positive neuron ratio in section where nuclei were stained with DAPI. Data are expressed as mean ± SEM (n = 5; 5 animals per group i.e., 10 ganglia were analyzed per genotype).