THE K+-EVOKED RELEASE OF (H-3)ACETYLCHOLINE FROM SLICES OF RAT GLOBUS-PALLIDUS - MODULATION BY DELTA-OPIOID RECEPTORS

Previous investigations have shown that the activation of delta-opioid receptors depresses the release of acetylcholine (ACh) in the rat caudate putamen. This finding raised the possibility that the release of ACh is similarly modulated in the globus pallidus, a region containing a distinct population of cholinergic neurons and enriched in enkephalinergic nerve terminals. In the present study the pallidal release of ACh was characterized and the effects of delta-opioid receptor activation on this release were examined. The results show that this release is stimulated by high K+ in a concentration- and Ca2+-dependent manner. D-Pen2, L-Pen5-enkephalin (0.1 - 10-mu-M), a selective delta-opioid receptor agonist, produced a dose-related inhibition of the 25 mM K+-evoked tritium release. The maximal inhibitory effect, representing a 34% decrease in the K+-induced tritium release, was observed at a concentration of 1-mu-M. This opioid effect was attenuated by the selective delta-opioid receptor antagonist, ICI 174864 (1-mu-M). These findings support the role of a delta-opioid receptor in the modulation of ACh release in the rat globus pallidus.