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. Author manuscript; available in PMC: 2020 Dec 1.
Published in final edited form as: Psychoneuroendocrinology. 2019 Sep 18;110:104439. doi: 10.1016/j.psyneuen.2019.104439

Fig. 5.

Fig. 5.

Expression of hyperactivity-related genes.Mice were injected with tamoxifen (KO/Act+ (tam)) or vehicle (KO/Act+ (oil)) at two months of age, and tissues were collected at six months of age. Baseline cortical, hypothalamic and striatal expression of Bdnf1, Cnr1, Grm5, and Snap25 in untreated females or male mice with or without Dio3 inactivation (A) or in animals treated with T3 (B). Data were normalized to values in KO/Act+ (oil) female mice. Data in (B) are represented as a fold change over the corresponding group of untreated animals (dotted line). Data are shown as mean ± SEM with n=6–8 mice per experimental group (A) or 3–5 mice (B) per experimental group. *, **, *** indicate P<0.05, P<0.01, P<0.001 statistical differences, respectively, between genotypes (black asterisks) or sexes (red asterisks). #, ##, ### indicate P<0.05, P<0.01, P<0.001 statistical differences, respectively, between T3-treated and untreated mice within a given genotype and sex. Statistical significance was determined by two-way ANOVA followed by Tukey’s multiple comparison test for multiple comparisons.