TrkB.T1 deletion induces cardiac pathological alterations coupled with an increase in L-type Ca²⁺ channel level and currents. (A) WT and TrkB.T1^−/− hematoxylin and eosin–stained transversal heart sections showing left ventricle dilation and reduced thickness of left ventricle posterior wall apparent in TrkB.T1-deficient animals. (B) Quantification of the thickness (arrow) of the posterior wall (PW) and left ventricle area (LV); RV, right ventricle; n = 4 for each genotype. (C) Representative echocardiography recording in M-mode obtained in WT and T1^−/− mice showing the left ventricle internal dimension at diastole (double head red arrows, LVID) and the left ventricle posterior wall (LVPW) thickness delineated by blue lines. (D) Quantification of LVID and LVPW thickness measured at diastole (dia), and fractional shortenings (FS) values obtained from the echocardiography recordings (P < 0.05). WT, n = 4; T1^−/−, n = 5. (E–J) TrkB.T1 deletion increases L-type calcium levels and currents in adult isolated cardiomyocytes. (E) I/V curves obtained in whole cell patch-clamp isolated adult cardiomyocytes showing similar activation of L-type calcium channels but higher current density in T1^−/− versus WT cardiomyocytes. (F) Channel kinetics and current decay recordings are comparable in T1^−/− and WT cardiomyocytes. (G) Measurements of plasma membrane capacitance are similar between WT and T1^−/− cardiomyocytes, suggesting no difference in cell size. (H) Graph showing similar calcium-induced L-type current inactivation calculated by paired pulse protocol in WT and T1^−/− cardiomyocytes. (I) Representative Western blot analysis of cardiac lysates from WT and T1^−/− hearts using an antibody specific for the α 1c subunit of the Cav1.2 channel. (J) Quantification of Western blot CaV1.2 a1c band intensity in relation to GAPDH; n = 6. Data are indicated as the mean ± SEM. *, P < 0.05.