The possible role of voltage-sensitive calcium channels (VSCC) activation in the glufosinate ammonium (GLA)-induced dopamine release was investigated using selective VSCC blockers and the dopamine levels were measured by HPLC from samples obtained by in vivo cerebral microdialysis. While pretreatment with 10 μM flunarizine (T-type VSCC antagonist) or nicardipine (L-type VSCC antagonist) had no statistically significant effect on dopamine release induced by 10 mM GLA, pretreatment with 100 μM of both antagonists, or 20 μM ω-conotoxin MVIIC (non-selective P/Q-type VSCC antagonist) significantly decreased the GLA-induced dopamine release over 72.2%, 73%, and 70.2%, respectively. Administration of the specific antagonist of neuronal N-type VSCCs, the ω-conotoxin GVIA (20 μM), produced an almost complete blockade of in vivo dopamine release induced by GLA. These results show that GLA-induced dopamine release could be produced by the activation of a wide range of striatal VSCC located at the synaptic terminals and axons of striatal dopaminergic neurons, especially N-type VSCC.
Keywords: Cerebral microdialysis; Glufosinate ammonium; Striatum; Voltage-sensitive calcium channels; in vivo dopamine release.
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