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

摘要: The aim of this study is to analyze further the opioid receptor subtypes involved in augmentation behavioral activity after dopamine depletion nucleus accumbens rats. Initially, receptors locomotion produced by endogenous opioids were evaluated microinjection kelatorphan, an inhibitor proteolytic enzymes that inactivates enkephalin, with or without specific antagonists forμ1 orδ-opioid receptors, naloxonazine naltrindole, respectively. Kelatorphan a dose-dependent increase horizontal photocell counts and vertical movements. At all doses examined response was augmented rats sustaining accumbal lesions. dopamine-depleted partially blocked naltrindole. Since motor stimulant intra-accumbens theδ-opioid agonist, [d-penicillamine2,5]-enkephalin, not previous study, we tested new endogenousδ-opioid [d-Ala2] deltorphin I. locomotor slightly These data suggest elicited lesions involves bothμ1 andδ-opioid receptors.