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. Author manuscript; available in PMC: 2012 Sep 21.
Published in final edited form as: J Neurosci. 2012 Mar 21;32(12):4065–4079. doi: 10.1523/JNEUROSCI.6314-11.2012

Figure 7.

Figure 7

Loss of ERK activation in BFCNs of TrkAcKO mice. A, p-ERK immunostaining in BF. At P9, weak activation of ERK was observed in both control and TrkAcKO (arrowheads) BF. By P14, stronger ERK activation, mostly limited to ChAT-positive neurons, was observed in control, but not in TrkAcKO MS. B,C, Immunoblot (B) and quantification (C) of ERK activation in BF tissue lysates of control or TrkAcKO mice. n=4 per genotype in each group; *p<0.05, **p<0.01. D,E, Absence of AKT activation in BFCNs as determined by immunofluorescence (D) and western blot (E) analyses. Although weak activation of AKT was observed in both control and mutant mice MS at P14 as measured by p-AKT immunofluorescence, it did not co-localize with ChAT-positive neurons and was no longer present at P30. Consistent with this, pAKT signal was undetectable in BF tissue lysates by western blots (E). In (E), cortex tissue lysates of control mice were used as the positive control; n=3. Scale bars: A, D, 50 μm.