Specific deletion of TrkB.T1 in cardiomyocytes abolishes BDNF inotropic effect and leads to cardiomyopathy. (A–C) Representative traces of LVDP before (baseline considered as 100%) and after BDNF or caffeine injection (arrows) in control myosin 6–specific cre transgenic (myh6-cre) mice used as controls (A), double Myh6-cre, TrkB.T1 conditional (Myh6-cre/TrkB.T1loxP; B), and endothelial-specific cre (Cdh5-cre) TrkB.T1 conditional (Cdh5-cre/TrkB.T1loxP; C) mutant mice. Caffeine was injected 5 min after BDNF as a positive control as in Fig. 2. The BDNF and caffeine traces were overlapped using the injection time (arrow) as a starting point. (D–F) Quantification of LVDP recorded from the mice in A (D), B (E), and C (F). (G–I) Cardiomyocyte-specific deletion of TrkB.T1 or BDNF causes dilated cardiomyopathy. Representative hematoxylin and eosin–stained sections from 2–3-mo-old control Myh6-cre transgenic (G; myh6; n = 4), Myh6-cre/BDNFloxP/loxP (H; Myh6-BDNF; n = 5), or Myh6-cre/TrkB.T1loxP/loxP (I; Myh6-TrkB.T1; n = 5) mouse hearts showing dilated left ventricle and reduced left ventricle posterior wall thickness caused by BDNF or TrkB.T1 deletion. (J and K) Quantification of left ventricle (LV) area and posterior wall (PW) thickness was measured in heart transverse sections at the level and in between the papillary muscles (arrow). RV, right ventricle. Data are indicated as the mean ± SEM. *, P < 0.05.
