Fig. 6
Ca2+ influx through L-type Ca2+ channels mediates Hebbian LTP at LPP-GC synapses. A Left & Middle, Representative AP responses to somatic rheobase current injection before (red, Con) and after application of nimodipine (purple, Nimo, 10 μM). Right, Finit of intrinsic bursts was not affected by nimodipine (Con, 198.3 ± 26.8 Hz; Nimo, 206.7 ± 36.0 Hz; n = 5). B Exemplar traces (left) and mean areas (right) of EPSP summation evoked by HFSL-2 of LPP before and after applying nimodipine (Con, 2.1 ± 0.3 mV s; Nimo, 2.3 ± 0.4 mV s; n = 6). C Exemplar voltage response of BS-GCs (left) evoked by HFSH-2 and mean Finit (right) in the presence of nimodipine (Nimo, 154.8 ± 17.5 Hz, n = 5). Black dashed line on the bar graph, control mean Finit in BS cells (128.3 Hz). D Left, Time course of normalized EPSP in BS-GCs before and after HFSH-2. Right, Magnitudes of early (LTP5, open circle) and late phase (LTP30, closed circle) LTP in control and nimodipine conditions (Con, n = 7; Nimo, n = 6). The control LTP time course and magnitudes were reproduced from Fig. 3D (light red). E Similar as in C, D, but applied a pairing protocol instead of HFSH. The control LTP trace and magnitudes were reproduced from Fig. 3H (gray) (Con, n = 14; Nimo, n = 7). F Time course of normalized EPSP in RS- and BS-GCs before and after HFSH-1. G Left, Time course of normalized EPSP in BS-GCs before and after HFSH-1 in the presence of nimodipine. Right, Magnitudes of late phase LTP (LTP30, closed circles). Note little effect of nimodipine on HFSH-1-induced LTP in BS-GCs. Shades and error bars, S.E.M. *p < 0.05. **p < 0.01. n.s., not significant (p > 0.05)