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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Dev Neurobiol. 2018 Aug 31;78(11):1117–1130. doi: 10.1002/dneu.22634

Figure 5:

Figure 5:

Western blot quantification of post-PTZ expression of TrkB and p-TrkB (T816), PLCγ, p-PLCγ (T783). (A) Representative western blots for TrkB, p-TrkB (T816) and their respective actins. (B-C) TrkB and p-TrkB (T816) expression remained stable, indicating no activation of TrkB pathway. (D – E) Ratio of p-TrkB (T816)/ TrkB of 24h and 2h post-PTZ, respectively, showed no significant changes. (F) Mean TrkB and p-TrkB (T816) percent of control shows no activation of TrkB pathway. (G) Representative western blots for PLCγ, p-PLCγ (T783) and their respective actins (H-I) PLCγ and p-PLCγ (T783) expression showed no significant differences at 24h. (J-K) Ratio of p-PLCγ (T783) to total PLCγ of 24h and 2h post-PTZ pups showed significant increase in +PB group at 24h. (L) At 2h, mean p-PLCγ (T783) percent of control shows significant increase (50%) in PTZ group compared to control and PLCγ shows significant increase compared to control (50%) in +PB group. At 24h, p-PLCγ (T783) percent of control in +PB group showed a significant reduction compared to controls (45%). There was also an additional significant difference in PLCγ in PTZ only and +PB treatment groups. Sample size: n=32 for 24h data, n=20 for 2h data. Between groups: #P < 0.05, ##P < 0.01, ###P ≤ 0.001, independent t-tests & one-way ANOVA with Bonferroni post-hoc correlations.