Field recordings were used to determine the influence of delta-opioid receptor activation on corticostriatal synaptic transmission. Application of the selective delta-opioid receptor agonist, [Tyr-D-Pen-Gly-Phe-D-Pen]-enkephalin (DPDPE, I mu M), 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 I nM of the selective delta-receptor antagonist naltrindole. Neither omega-conotoxin GVIA (1 mu M) nor omega-agatoxin TK (400 nM), blockers of N- and P/Q-type Ca2+-channels, respectively, nor TEA (I mM), blocker of some classes of K+-channels, occluded the effects of DPDPE. Instead, I mM 4-AP or 400 mu M Ba2+, occluded completely the effects of DPDPE. Therefore, the results suggest that the modulation by delta opioids at corticostriatal terminals is mediated by transient (K(v)4) K+-conductances. (c) 2006 Published by Elsevier Ireland Ltd.
Última actualización: 23/02/2018