Abstract
We examined the properties of voltage-dependent Ca 2+ channels (VDCCs) mediating 1-methyl-4-phenylpyridinium (MPP +)-evoked [ 3H]DA release from rat striatal slices. In some cases, the Ca 2+-independent efflux of neurotransmitters is mediated by the high-affinity neurotransmitter-uptake systems. To determine whether such a mechanism might be involved in MPP +-evoked [ 3H]DA release. MPP + (1, 10 and 100 μM) evoked the release of [ 3H]DA from rat striatal slices in a concentration-dependent manner. In the absence of Ca 2+, MPP + (10 and 100 μM)-evoked [ 3H]DA release was significantly decreased to approximately 50% of control (a physiological concentration of Ca 2+). In the presence of Ca 2+, nomifensine (0.1, 1 and 10 μM) dose-dependently and significantly inhibited the MPP +-evoked release of [ 3H]DA. Nomifensine (1 and 10 μM) also dose-dependently and significantly inhibited the MPP +-evoked release of [ 3H]DA under Ca 2+-free conditions. MPP +-evoked [ 3H]DA release was partly inhibited by nicardipine (1 and 10 μM), an L-type Ca 2+ channel blocker. On the other hand, the N-type Ca 2+ channel blocker ω-conotoxin-GVIA (ω-CTx-GVIA) (1 and 3 μM) did not affect this release. ω-agatoxin-IVA (ω-Aga-IVA) at low concentrations (0.1 μM), which are sufficient to block P-type Ca 2+ channels alone, also had no effect. On the other hand, MPP +-evoked [ 3H]DA release was significantly decreased by high concentrations of ω-Aga-IVA (0.3 μM) that would inhibit Q-type Ca 2+ channels. In addition, application of the Q-type Ca 2+ channel blocker ω-conotoxin-MVIIC (ω-CTx-MVIIC) (0.3 and 1 μM) also significantly inhibited MPP +-evoked [ 3H]DA release. These results suggest that MPP +-evoked [ 3H]DA release from rat striatal slices is largely mediated by Q-type Ca 2+ channels, and the Ca 2+-independent component is mediated by reversal of the DA transport system.
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