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Dopamine depletion augments endogenous opioid-induced locomotion in the nucleus accumbens using bothμ1 andδ opioid receptors

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Abstract

The aim of this study is to analyze further the opioid receptor subtypes involved in the augmentation of behavioral activity after dopamine depletion in the nucleus accumbens of rats. Initially, the opioid receptors involved in the augmentation of locomotion produced by endogenous opioids were evaluated by microinjection of kelatorphan, an inhibitor of proteolytic enzymes that inactivates enkephalin, with or without specific antagonists forμ 1 orδ-opioid receptors, naloxonazine or naltrindole, respectively. Kelatorphan produced a dose-dependent increase in horizontal photocell counts and vertical movements. At all doses examined the behavioral response was augmented in rats sustaining accumbal dopamine lesions. The augmentation in dopamine-depleted rats was partially blocked by naloxonazine or naltrindole. Since the motor stimulant response to intra-accumbens microinjection of theδ-opioid agonist, [d-penicillamine2,5]-enkephalin, was not augmented in a previous study, we tested the behavioral response to a new endogenousδ-opioid agonist, [d-Ala2] deltorphin I. The locomotor response to deltorphin was slightly augmented in dopamine-depleted rats. These data suggest that the augmentation in the motor response elicited by endogenous opioids after dopamine lesions in the nucleus accumbens involves bothμ 1 andδ-opioid receptors.

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Churchill, L., Roques, B.P. & Kalivas, P.W. Dopamine depletion augments endogenous opioid-induced locomotion in the nucleus accumbens using bothμ1 andδ opioid receptors. Psychopharmacology 120, 347–355 (1995). https://doi.org/10.1007/BF02311183

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