Fig. 2: Reactivation of the mutant TRα1 with T3 and central T3 i.c.v. administration at 30 °C. | Nature Communications

Fig. 2: Reactivation of the mutant TRα1 with T3 and central T3 i.c.v. administration at 30 °C.

From: Resistance to thyroid hormone induced tachycardia in RTHα syndrome

Fig. 2: Reactivation of the mutant TRα1 with T3 and central T3 i.c.v. administration at 30 °C.The alternative text for this image may have been generated using AI.

a Radiotelemetry recordings of heart rate in TRα1 + m (red) as well as wild-type controls (black) over 12 days of oral T3 treatment at 30 °C. Black bars indicate dark time activity period. b Contributions of the parasympathetic (PSNS) or sympathetic nervous system (SNS) in these animals as determined by change in heart rate upon pharmacological blockade with methylscopolamine or timolol at 30 °C before and after 12 days of T3 treatment. c Intrinsic heart rate after full pharmacological blockade in these animals at 30 °C before and after 12 days of T3 treatment. d Development of heart rate distribution over 11 consecutive days of T3 treatment at 30 °C in these animals. e Heart rate in wild-type or TRα1 + m (f) animals after i.c.v. injection of 8 ng T3 (black or orange) or control solution (green or red) as recorded by radiotelemetry for 6 h at 30 °C. Values are mean ± SEM for n = 4 wild-type controls and n = 7 TRα1 + m mutants; n = 5 wild-types and n = 3 TRα1 + m mutants for i.c.v. study. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 with two-way ANOVA and Sidak’s multiple comparison tests. Exact P values are provided in Supplementary Table 1.

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