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(ol)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 μ-opiate agonists (morphine and DAGO) on ACh release evoked by K+ was sensitive to tetrodotoxin (TTX), but that of δ-opiate agonists (DADLE and DPDPE) was insensitive. The release evoked by GLU was abolished in the presence of TTX. The activation of κ-opiate receptor by dynorphin-(1-13) had no effect on K+- or GLU-evoked ACh release. It is concluded that μ- and δ-opiate agonists, but not κ, exert an inhibitory control on striatal cholinergic interneurons, but with a different mechanism of action or localization of the receptors. Corticostriatal glutamatergic neurons have an important role in the interaction of the ACh-opioid systems. © 1990.