• Sergio Recillas-Morales, Lizzette Sánchez-Vega, Norma Ochoa-Sánchez, Isaac Caballero-Florán, Francisco Paz-Bermúdez, Isaac Silva, Jorge Aceves, David Erlij, and Benjamín Florán.
• Department of Pharmacology, CINVESTAV-IPN, México.
• Neuroscience. 2013 Oct 26.

AbstractModulation of L-type Ca(2+)-channel function by dopamine is a major determinant of the rate of action potential firing by striatal medium spiny neurons (MSNs). However, the role of these channels in modulating GABA release by nerve terminals in the basal ganglia is unknown. We found that depolarization induced [(3)H]GABA release in both the substantia nigra reticulata and the external globus pallidus, was depressed by about 50% by either the selective L-channel dihydropiridine blocker nifedipine or the P/Q channel blocker ω-agatoxin TK. The effects of these blockers were additive and together eliminated about 90% of depolarization induced [(3)H]GABA release. In addition, in the substantia nigra reticulata, dihydropyridines prevented both the stimulation of [(3)H]GABA release produced by dopamine D1 receptor activation and the inhibition caused by D4 receptor activation. In the globus pallidus nifedipine blocked the effects of D2 and A2A receptor coactivation as well as the effects of activating adenylyl cyclase with forskolin. ω-agatoxin TK did not interfere with the action of these modulatory agents. The L-type Ca(2+)-channel agonist BAYK 8644 stimulated GABA release in both substantia nigra reticulata and globus pallidus. Because dihydropiridine sensitivity is a key criteria to identify L-type Ca(2+)-channel activity, our results imply that these channels are determinant of GABA release modulation by dopamine in striatonigral, striatopallidal and pallidonigral terminals.Copyright © 2013. Published by Elsevier Ltd.

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