Voltage-activated calcium channels involved in veratridine-evoked [3H]dopamine release in rat striatal slices

The present study explored the role of different sub-types of voltage-activated Ca2+ channels (VACCs) in mediating veratridine-evoked [H-3]dopamine (DA) release from rat striatal slices. The release of [H-3]DA evoked by veratridine (25 mu M) decreased by 50.6 +/- 2.9% (n = 8) in the absence of calcium and was completely abolished by 1 mu M tetrodotoxin. The L-type Ca2+ channel blockers nifedipine (10 mu M), nitrendipine (10 mu M), diltiazem (10 mu M) and verapamil (IO mu M) did not modulate this release. Similarly, [H-3]DA release was affected neither by the N-type VACC blocker omega-conotoxin-GVIA (I mu M) nor by the selective P-type channel blockers omega-agatoxin-IVA and omega-agatoxin-TK at low nM concentrations (30 nM), indicating no involvement of N- and P-type Ca2+ channels. In contrast, higher concentrations of w-agatoxin-IVA that would also inhibit Q-type VACCs, blocked the release of [H-3]DA by 27.9 +/- 8.1% (n = 5) and 37.5 +/- 13.6% (n = 3) at 0.3 and 1 mu M, respectively. In addition, application of the Q-type Ca2+ channel blocker omega-conotoxin-MVIIC (0.01-3 mu M) reduced [H-3]DA release in a concentration-dependent manner, with maximum inhibition of 35.3 +/- 4.1% at 3 mu M (n = 5). On the basis of these results, it is concluded that the Ca2+ channels that participate in veratridine-evoked [3H]DA release are Q-type Ca2+ channels. (C) 1998 Elsevier Science Ltd. All rights reserved.