Fig. 5
From: Effects of early-life exposure to THIP on phenotype development in a mouse model of Rett syndrome
THIP administration suppressed the hyperexcitability of LC neurons in MECP2-null mice. A 1 , A 2 Typical recordings of spontaneous firing of LC neurons in WT and MECP2-null mice at 1 month of age without THIP treatment. B 1 , B 2 Spontaneous firing of LC neurons in WT and MECP2-null mice of the same age with THIP pretreatment. C–F THIP administration did not significantly change membrane potentials, input resistance, action potential overshoot, and action potential threshold in both WT and MECP2-null mice. No significant main effect of THIP treatment (F = 0.09, df = 1, P = 0.765; F = 1.15, df = 1, P = 0.289; F = 0.27, df = 1, P = 0.606; F = 0.76, df = 1, P = 0.387; C, D, E, F, respectively) and genotype (F = 1.45, df = 1, P = 0.234; F = 0.09, df = 1, P = 0.765; F = 0.01, df = 1, P = 0.921; F = 0.99, df = 1, P = 0.324; C, D, E, F, respectively) were observed, either the interaction (F = 0, df = 1, P = 1.000; F = 1.46, df = 1, P = 0.232; F = 0.03, df = 1, P = 0.863; F = 3.58, df = 1, P = 0.064; C, D, E, F, respectively). G The main effect of genotype was significant (F = 10.06, df = 1, P < 0.01), whereas the main effect of THIP treatment was not (F = 1.72, df = 1, P = 0.196). The interaction of these two factors was significant (F = 8.6, df = 1, P < 0.01) as well (## P < 0.01; two-way ANOVA). The firing activity of LC neurons in MECP2-null mice is significantly increased compared to the WT and chronic treatment with THIP abolished the hyperexcitability (vehicle: n = 14 and n = 13; THIP: n = 13 and n = 16; in WT and MECP2-null, respectively; ***P < 0.001; Tukey’s post hoc)