Effect of opioids on acetylcholine release evoked by K+ or glutamic acid from rat neostriatal slices

Endogenous acetylcholine (ACh) release from rat striatal slices was measured by a chemiluminescent method. Several opiate agents were tested for their ability to modulate ACh release evoked by potassium ions (K+) or glutamic acid (GLU). Morphine, [D-Ala2,Gly(0l)5]-enkephalin (DAGO), [D-Ala2,D-Leu5]-enkephalin (DADLE) and [D-Pen2-D-Pen5]-enkephalin (DPDPE) were found to have an inhibitory effect on K(+)- or GLU-evoked ACh release. This effect was completely blocked by naloxone, but this antagonist by itself had no effect on ACh release. The action of mu-opiate agonists (morphine and DAGO) on ACh release evoked by K+ was sensitive to tetrodotoxin (TTX), but that of delta-opiate agonists (DADLE and DPDPE) was insensitive. The release evoked by GLU was abolished in the presence of TTX. The activation of kappa-opiate receptor by dynorphin-(1-13) had no effect on K(+)- or GLU-evoked ACh release. It is concluded that mu- and delta-opiate agonists, but not kappa, exert an inhibitory control on striatal cholinergic interneurons, but with a different mechanism of action of localization of the receptors. Corticostriatal glutamatergic neurons have an important role in the interaction of the ACh-opioid systems.