Fig. 3: Decreased phosphorylation of CREB and PKA substrates in RIIβ-/- mice, and RIIβ null exhibited anticonvulsant activity in KA-induced mouse experimental seizure model.
From: PKA-RIIβ autophosphorylation modulates PKA activity and seizure phenotypes in mice

a Western blot analysis showed p-CREB, total CREB, and p-PKA substrates protein levels in the DG, CA1, CA3 area, and entorhinal cortex (EC) from WT and RIIβ−/− mice. b–d Quantification of the Western blot results in a n = 5 mice for each group, *P < 0.05; **P < 0.01; ***P < 0.001, unpaired two-tailed Student’s t test. e Graph depicting limbic seizure progression, illustrated as mean maximum seizure class reached by 15, 30, 45, 60, or 90 min after kainic acid administration (30 mg/kg, i.p.) in WT (n = 8) and RIIβ−/− (n = 7) mice. P = 0.0014 at 15 min, P = 0.1636 at 30 min, P = 0.0107 at 45 min, P = 0.0145 at 60 min, P = 0.0145 at 90 min, ns no significance, P > 0.05; *P < 0.05; **P < 0.01 for each time bin, data were analyzed by unpaired two-tailed non-parametric Mann–Whitney U-test. f Incidence of maximum seizure Class reached during the course of the experiment. Data were represented as mean ± SEM.