Spikes population evoked by a paired pulse protocol were used to assess the influence of GABA(A) and GABA(B) receptors agonists and antagonists on the synaptic potentials and in the S2/S1 ratio in a paired pulse (PP) protocol in the cortico-paleostriatum augmentatum synapses of the turtle. GABA(A) agonist, muscimol, decreased the amplitude of synaptic responses whereas the facilitation produced with the PP protocol did not change, suggesting a postsynaptic action for GABA(A) receptors. GABA(B) agonist, baclofen, enhanced paired pulse ratio indicating a presynaptic modulation through the GABA(B) receptor. Selective antagonists for N- and P/Q-type Ca(2+)-channels also enhanced paired pulse ratio, suggesting that any of these channel types may be involved in neurotransmitter release. However, the strong paired pulse facilitation produced by baclofen was occluded by blocking the N-type Ca2+ channels with omega-conotoxin GVIA (1 microM), but not by the blockage of P/Q-type Ca2+ channels with omega-agatoxin TK (400 nM). These data suggest that N and P/Q channels participate in the neurotransmitter release, whereas only N-type Ca2+ channels are involved in the presynaptic modulation of GABA(B) in the corticostriatal synapse of the turtle.