Abstract
Endogenous acetylcholine (ACh) release from rat neostriatal slices were inhibited by the μ-opioid agonist [ d-Ala 2,Gly(ol) 5]-enkephalin (DAGO) both in 6-hydroxydopamine (6-OHDA)-lesioned and non-lesioned neostriatum. However, the δ-opioid agonist [ d-Pen 2, d-Pen 5]-enkephalin (DPDPE) could not inhibit KCl-evoked ACh release in the 6-OHDA-lesioned striatum. This results suggests that δ-opioid agonist act on dopaminergic terminals to inhibit the cholinergic neurons. In unlesioned rats, GABA A or GABA B antagonists (bicuculline or phaclofen, respectively) prevented μ- or δ-opioid inhibition of endogenous ACh release evoked by glutamate, but not by potassium. However, in the 6-OHDA-lesioned side, DAGO inhibition of KCl-evoked ACh release was antagonized by either of the GABA antagonists. Our results suggest that the dopaminergic neurotransmission, favored by KCl, blocks the GABAergic involvement in the μ- and δ-opioid inhibition of endogenous ACh release.
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