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. Author manuscript; available in PMC: 2014 Jul 10.
Published in final edited form as: Neuron. 2013 Jun 20;79(1):31–38. doi: 10.1016/j.neuron.2013.04.027

Figure 3. SE-induced hippocampal damage is attenuated by inhibition of TrkB kinase.

Figure 3

(A) Representative images of immunostaining of NeuN and GFAP in the hippocampal CA3b region ipsilateral to the infusion site in WT and TrkBF616A mice in respective PBS controls, SE-vehicle treated, and SE-1NMPP1 treated mice, scale bar = 50 µM. Insets: GFAP positive cells exhibited enhanced immunoreactivity and enlarged cell bodies and braches in SE-vehicle or 1NMPP1 treated WT mice and in SE-vehicle treated TrkBF616A mice, scale bar = 20 µM. (B) Number of NeuN positive cells within ipsilateral CA3b hippocampus was reduced in both WT and TrkBF616A mice undergoing SE and treated with vehicle thereafter compared to PBS controls (WT: ***p<0.001; TrkBF616A: ***p<0.001). 1NMPP1 treatment inhibited loss of NeuN positive cells in TrkBF616A mice (***p<0.001), but not in WT mice. Data are presented as mean ± SEM and analyzed using two-way ANOVA with Bonferroni post hoc tests, n=3–6.