Role of voltage-gated calcium channels on striatal dopamine release induced by inorganic mercury in freely moving rats.
The possible role of voltage-sensitive calcium channels (VSCC) activation on the HgCl2-induced dopamine release was investigated using selective VSCC blockers and the dopamine levels were measured by HPLC from samples obtained by in vivo brain microdialysis. Infusion of HgCl2 in nicardipine (10 or 100 μM) or flunaricine (10 μM) pretreated animals had no significant effect on dopamine release induced by HgCl2. Pretreatment with 100 μM flunaricine, 20 μM ω-conotoxin MVIIC, or ω-conotoxin GVIA significantly decreased the HgCl2-induced dopamine release over 61%, 88%, and 99%, respectively. HgCl2-induced dopamine release could be produced, at least in part, by activation of VSCC at dopaminergic terminals, especially N- and P/Q-type.
['Faro|Lilian R Ferreira|LRF|', 'Alfonso|Miguel|M|', 'Ferreira|Vania Moraes|VM|', 'Durán|Rafael|R|']
D000818:Animals D002121:Calcium Channel Blockers D015220:Calcium Channels D003342:Corpus Striatum D004298:Dopamine D005260:Female D005444:Flunarizine D008628:Mercury D009529:Nicardipine D017207:Rats, Sprague-Dawley D020866:omega-Conotoxin GVIA D020960:omega-Conotoxins
Dopamine release Inorganic mercury Voltage-sensitive calcium channels In vivo Calcium channels blockers.