

Author: Dobrev Dobromir Andreas Klaus
Publisher: Springer Publishing Company
ISSN: 0364-3190
Source: Neurochemical Research, Vol.22, Iss.9, 1997-09, pp. : 1085-1093
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Abstract
We examined the involvement of voltage-activated Ca2+ channels (VACCs) on K+(50 mM)-evoked [3H]dopamine ([3H]DA) release from superfused rat striatal slices. Neither nifedipine nor nitrendipine modified K+-evoked [3H]DA release, indicating that L-type VACCs are not involved. K+-evoked [3H]DA release was partially inhibited by ω-CTx-GVIA and ω-Aga-IVA, and was abolished by 3 μM ω-CTx-MVIIC (IC50 ∼128 nM), suggesting the involvement of N-, P-, or Q-type VACCs, respectively. Moreover, even subnanomolar concentrations of ω-CTx-MVIIC (0.1–0.5 nM) inhibited K+-evoked [3H]DA release by ∼25%, suggesting the possible involvement of a still not classified (perhaps O-type?) Ca2+ channel subtype. The effects of ω-CTx-MVIIC (10–100 nM) and ω-CTx-GVIA (1 μM) were additive, suggesting that low nanomolar concentrations of ω-CTx-MVIIC does not interact with N-type VACCs. In conclusion, the K+-evoked [3H]DA release from rat striatal slices is mediated by entry of Ca2+ through ω-CTx-GVIA sensitive (N-type) as well as through ω-Aga-IVA (P-type) and ω-CTx-MVIIC (probably Q-type) sensitive VACCs.
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