Modulation of potassium-evoked [H-3]dopamine release from rat striatal slices by voltage-activated calcium channel ligands: Effects of omega-conotoxin-MVIIC

We examined the involvement of voltage-activated Ca2+ channels (VACCs) on K+(50 mM)-evoked [H-3]dopamine ([H-3]DA) release from superfused rat striatal slices. Neither nifedipine nor nitrendipine modified K+-evoked [SH]DA release, indicating that L-type VACCs are not involved. K+-evoked [H-3]DA release was partially inhibited by omega-CTx-GVIA and omega-Aga-IVA, and was abolished by 3 mu M omega-CTx-MVIIC (IC50 similar to 128 nM), suggesting the involvement of N-, P-, or Q-type VACCs, respectively. Moreover, even subnanomolar concentrations of omega-CTx-MVIIC (0.1-0.5 nM) inhibited K+-evoked [H-3]DA release by similar to 25%, suggesting the possible involvement of a still not classified (perhaps O-type?) Ca2+ channel subtype. The effects of omega-CTx-MVIIC (10-100 nM) and omega-CTx-GVIA (1 mu M) were additive, suggesting that low nanomolar concentrations of omega-CTx-MVIIC does not interact with N-type VACCs. In conclusion, the K+-evoked [H-3]DA release from rat striatal slices is mediated by entry of Ca2+ through omega-CTx-GVIA sensitive (N-type) as well as through omega-Aga-IVA (P-type) and omega-CTx-MVIIC (probably Q-type) sensitive VACCs.