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Figure 3 | Molecular Brain

Figure 3

From: Genetic and pharmacological inhibition of calcineurin corrects the BDNF transport defect in Huntington's disease

Figure 3

FK506 restores transport alteration of BDNF-containing vesicles in cortical HdhQ111/Q111 mice neurons. (A and B) Cortical primary neurons from knock-in Huntington's disease mice model were electropored with BDNF-mCherry and incubated for 72 h. 1 h prior videomicroscopy experiment, neurons were treated with either DMSO or the following increasing concentrations of FK506 0.1 μM, 0.3 μM 1 μM or DMSO. FK506 induced a statistically significant increase in both anterograde and retrograde velocities with all the tested concentrations (Anterograde: **p < 0.01 for 0.1 μM, *p < 0.05 for 0.3 μM **p < 0.01 for 1 μM. Retrograde: ***p < 0.001 for 0.1 μM, *p < 0.05 for 0.3 μM **p < 0.01 for 1 μM). No significant differences were observed between the different concentrations. (C) FK506 treatment also reduced significantly the pausing time of BDNF-mCherry vesicles observed in HdhQ111/Q111 mice cortical neurons (**p < 0.01 for 0.1 μM, 0.3 μM and 1 μM FK506 concentrations). Data are from two independent experiments, 3736 tracks, 8 cells for HdhQ111/Q111 + DMSO, 4302 tracks, 10 cells for HdhQ111/Q111 + FK506 0.1 μM, 2959 tracks, 11 cells for HdhQ111/Q111 + FK506 0.3 μM, 2964 tracks, 8 cells for HdhQ111/Q111 + FK506 1 μM. (D) Representative kymographs of BDNF-mCherry dynamics in cortical neurons from HdhQ111/Q111mice treated with DMSO (upper kymograph) or 1 μM FK506 during 30 min (lower kymograph).

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