δ Opioids reduce the neurotransmitter release probability by enhancing transient (KV4) K+-currents in corticostriatal synapses as evaluated by the paired pulse protocol

Field recordings were used to determine the influence of δ-opioid receptor activation on corticostriatal synaptic transmission. Application of the selective δ-opioid receptor agonist, [Tyr-D-Pen-Gly-Phe-D-Pen]-enkephalin (DPDPE, 1 μM), decreased the amplitude of the field-excitatory synaptic potential and at the same time increased the paired pulse ratio (PPR) suggesting a presynaptic site of action. This response reversed rapidly when DPDPE was washed and blocked by 1 nM of the selective δ-receptor antagonist naltrindole. Neither ω-conotoxin GVIA (1 μM) nor ω-agatoxin TK (400 nM), blockers of N- and P/Q-type Ca2+-channels, respectively, nor TEA (1 mM), blocker of some classes of K+-channels, occluded the effects of DPDPE. Instead, 1 mM 4-AP or 400 μM Ba2+ occluded completely the effects of DPDPE. Therefore, the results suggest that the modulation by δ opioids at corticostriatal terminals is mediated by transient (KV4) K+-conductances.