“…Moreover, enhanced EPSC amplitudes were not owing to changes of the readily releasable pool of SVs, as revealed by hypertonic sucrose applications, inducing Ca 2 þ -independent release [20] (charge transfer, wt ¼ 1.59 ± 0.23 nC; het ¼ 1.71 ± 0.23 nC, Fig 2E). Finally, the charge transfer at glutamatergic synapses induced by 40 mM calcimycin, which causes calcium-dependent exocytosis bypassing activation of VGCCs [21], was lower, although not significantly, in het neurons with respect to wt (wt ¼ 0.29± 0.38 nC, het ¼ 0.22±0.57 nC, Fig 2F), suggesting a requirement of presynaptic calcium channels in the SNAP-25-dependent effects.…”