Figure 2. TrkB.T1 mediates BDNF-induced acute increase in cardiac contraction force and calcium transient increase evoked by direct stimulation in cardiomyocytes. (A and B) BDNF (1 ng in 50 µl Krebs solution) injected in the fluid streamline of a Langendorff-perfused mouse heart induces an increase in systolic pressure and a consequent decrease of the diastolic pressure (A) that is not affected by the TrkB kinase inhibitor K252a (B), Arrows indicate the time of BDNF injection and the broken line (B) indicates K252a presence throughout the 80-s duration of the experiment. (C) Representative traces showing the changes in LVPD before (baseline) and after BDNF injection. (D) Representative traces showing the changes in LVPD before (baseline) and after BDNF injection in the presence of 200 µM K252A. (E and F) Representative traces showing the increase in LVDP caused by BDNF in WT (E) but not in TrkB.T1 knockout (T1−/−; F) hearts. A bolus of 50 µl of 5 mM caffeine in Krebs solution was injected 5 min after BDNF as a positive control. The BDNF and caffeine traces were overlapped using the injection time as the starting point (arrow). Note the lack of LVDP change in response to BDNF in the TrkB.T1 mutant mouse despite normal response to caffeine. (G and H) Quantification of data in E and F showing the percent change of baseline LVPD in response to BDNF (G) and caffeine (H) in WT and T1−/− hearts. (I) Representative traces of Ca2+ transients elicited by 2-Hz stimulation in isolated adult cardiomyocytes. Ca2+ transient are increased by BDNF application only in WT (BDNF, light gray; no BDNF, black) but not in T1−/− cardiomyocytes. (J) Effect of BDNF on transient amplitude is reversible as shown in typical time course from a WT and a T1−/− cardiomyocyte. BDNF effect on Ca2+ release has a rapid onset and is completely reversed in <2 min upon BDNF removal. (K) Quantification of peak amplitude of calcium transient in WT and T1−/− cardiomyocytes. The value for each group represents the transient change in percentage before (considered as 100%) and after BDNF application. 10 transients before and 10 transients after BDNF application were measured for each cardiomyocyte analyzed (n is shown within the bar). Values in G–K are indicated as the mean ± SEM. *, P < 0.05.
Figure 2.

TrkB.T1 mediates BDNF-induced acute increase in cardiac contraction force and calcium transient increase evoked by direct stimulation in cardiomyocytes. (A and B) BDNF (1 ng in 50 µl Krebs solution) injected in the fluid streamline of a Langendorff-perfused mouse heart induces an increase in systolic pressure and a consequent decrease of the diastolic pressure (A) that is not affected by the TrkB kinase inhibitor K252a (B), Arrows indicate the time of BDNF injection and the broken line (B) indicates K252a presence throughout the 80-s duration of the experiment. (C) Representative traces showing the changes in LVPD before (baseline) and after BDNF injection. (D) Representative traces showing the changes in LVPD before (baseline) and after BDNF injection in the presence of 200 µM K252A. (E and F) Representative traces showing the increase in LVDP caused by BDNF in WT (E) but not in TrkB.T1 knockout (T1−/−; F) hearts. A bolus of 50 µl of 5 mM caffeine in Krebs solution was injected 5 min after BDNF as a positive control. The BDNF and caffeine traces were overlapped using the injection time as the starting point (arrow). Note the lack of LVDP change in response to BDNF in the TrkB.T1 mutant mouse despite normal response to caffeine. (G and H) Quantification of data in E and F showing the percent change of baseline LVPD in response to BDNF (G) and caffeine (H) in WT and T1−/− hearts. (I) Representative traces of Ca2+ transients elicited by 2-Hz stimulation in isolated adult cardiomyocytes. Ca2+ transient are increased by BDNF application only in WT (BDNF, light gray; no BDNF, black) but not in T1−/− cardiomyocytes. (J) Effect of BDNF on transient amplitude is reversible as shown in typical time course from a WT and a T1−/− cardiomyocyte. BDNF effect on Ca2+ release has a rapid onset and is completely reversed in <2 min upon BDNF removal. (K) Quantification of peak amplitude of calcium transient in WT and T1−/− cardiomyocytes. The value for each group represents the transient change in percentage before (considered as 100%) and after BDNF application. 10 transients before and 10 transients after BDNF application were measured for each cardiomyocyte analyzed (n is shown within the bar). Values in G–K are indicated as the mean ± SEM. *, P < 0.05.

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