1. Voltage-dependent facilitation of Ca2+ channels was studied in acutely isolated adult rat neostriatal neurons. Particular attention was paid to the facilitation of L-type channels. 2. In the absence of neuromodulators, the current-voltage relationship for whole cell Ba2+ currents was enhanced by a prepulse to +100 mV. The median enhancement at -20 mV was nearly 60%. The voltage dependence and kinetics of the processes underlying the facilitation were similar to those reported in other neurons. N-, P-, Q-, and L-type currents contributed to the observed facilitation. 3. Voltage dependent facilitation of L-type currents was studied by subtracting nifedipine-insensitive currents from control currents. Although the kinetics were similar to those of the whole cell currents, the half-activation voltage for facilitation of L-type currents [half-activation voltage (V(h)) = 0.6 mV, slope factors (V(c)) = 11.8 mV, n = 51 was significantly less depolarized than that of the pooled currents (V(h) = 47.3 mV, V(c) = 12.3 mV, n = 7). 4. Repetitive depolarization with spikelike waveforms was also able to induce facilitation of L-type currents, arguing that this process was of physiological significance. 5. The L channel agonist Bay K 8644 failed to occlude voltage-dependent facilitation of L-type currents, suggesting that facilitation was not simply a consequence of a modal shift in gating like that induced by Bay K 8644. 6. Combined whole cell recording and single-cell reverse transcription-polymerase chain reaction amplification revealed that neostriatal medium spiny neurons expressed detectable levels of either class C or class D L-type channel α1 subunit mRNA. Both neurons expressing class C L type channels and neurons expressing class D L-type channels exhibited voltage-dependent facilitation.
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