Figure 1. Developmental changes in I_pCa inactivation at the calyx of Held.

I_pCa was induced by paired depolarizing command pulses (from −80 mV to 0 mV, 1 ms in duration) in P7–9 (A and B) or P13–15 (C and D) rat calyces. A and C, sample records of I_pCa after application of calmidazolium (Calm. 20 μm by preincubation), or MLCK peptide (MLCK, 30 μm, by intraterminal application), or without application of CaM inhibitors (Control). The fist and second I_pCa are superimposed on the right panel at faster time scales. Dashed lines indicate the first I_pCa amplitudes. B and D, the ratio of the second I_pCa amplitude relative to the first one (I_pCa ratio on ordinate) at different ISIs (abscissa) after calmidazolium treatment (•), intraterminal application of MLCK peptide (▴) or with no inhibitor application (○). At P7–9 (B), maximal I_pCa inactivation (at 0.5 s ISI) was 15.6 ± 2.4% (n = 6) in control, 6.4 ± 0.6% (n = 5) after calmidazolium treatment, and 3.7 ± 1.1% (n = 5) after intraterminal MLCK peptide application. At P13–15 (D), maximal I_pCa inactivation (at 50 ms ISI) was 4.1 ± 0.7% (n = 7) in control, 2.8 ± 1.0% (n = 4) after calmidazolium treatment, and 1.5 ± 0.5% (n = 5) after intraterminal MLCK peptide application. Results were essentially the same when the charge instead of amplitude was measured for I_pCa. In this and following figures, data points and bars indicate mean and s.e.m.