GABAergic presynaptic inhibition of rat neostriatal afferents is mediated by Q-type Ca(2+) channels.

Population spikes associated with the paired pulse facilitation paradigm have been successfully used to measure presynaptic inhibition in several systems. In the present work, this paradigm was used to evaluate the action of baclofen on neostriatal glutamatergic transmission. Baclofen enhanced synaptic facilitation with an EC(50)=0.57 microM and a maximal effect of 457%. Selective antagonists for N-, P- and Q-type Ca(2+)-channels enhanced paired pulse facilitation; suggesting that these channel types participate in the release of transmitter. Nevertheless, neither 1 microM omega-conotoxin GVIA, nor 20 nM omega-agatoxinTK occluded the action of baclofen. Baclofen's action was occluded only by 400 nM omega-agatoxinTK. These data suggest that Q-type Ca(2+)-channels mediate gamma-aminobutyric acid(B) presynaptic inhibition of neostriatal afferents.