caa a22 4500 469119950 CHVBK 20180323133135.0 cr unu---uuuuu 170328e19920701xx s 000 0 eng 10.1007/BF02245299 doi (NATIONALLICENCE)springer-10.1007/BF02245299 Dopamine and endogenous opioid regulation of picrotoxin-induced locomotion in the ventral pallidum after dopamine depletion in the nucleus accumbens [Elektronische Daten] [Lynn Churchill, Mark Austin, Peter Kalivas] Microinjection of picrotoxin or the μ-opioid agonist, Tyr-D-Ala-Gly-NmePhe-Gly-OH (DAMGO), into the ventral pallidum (VP) produces an increase in locomotor activity that is antagonized by dopamine receptor blockade. To investigate the regulation of VP-induced locomotion by the dopaminergic innervation of the nucleus accumbens (NA) and the role of opioid receptors in this regulation, dopamine innervation of the NA was bilaterally lesioned with 6-hydroxydopamine (6-OHDA). The lesions resulted in an 89-97% depletion of tissue dopamine levels in the nucleus accumbens compared with sham-lesioned rats. Dopamine depletion in the NA failed to significantly antagonize picrotoxin or DAMGO injected into the VP. However, the dopamine receptor antagonist, haloperidol (0.1 mg/kg, IP), blocked the picrotoxin-initiated increase in horizontal photocell counts in both sham- and 6-OHDA-lesioned rats. The opioid receptor antagonist, naloxone (1.0 mg/kg, SC), also blocked the picrotoxin-induced locomotion in 6-OHDA-lesioned rats but did not block locomotion in the sham-lesioned rats. At a higher dose (3.0 mg/kg, SC), naloxone blocked picrotoxin-induced locomotion in both sham- and 6-OHDA-lesioned rats. These results indicate that although dopamine depletion in the NA does not affect the permissive role of dopamine transmission on locomotion elicited from the VP, it results in an increased sensitivity to enkephalinergic transmission. Springer-Verlag, 1992 Mesolimbic dopamine system nationallicence Opioid receptor nationallicence Haloperidol nationallicence Naloxone nationallicence Churchill Lynn Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut Austin Mark Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut Kalivas Peter Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut Psychopharmacology Springer-Verlag 108/1-2(1992-07-01), 141-146 0033-3158 108:1-2<141 1992 108 213 https://doi.org/10.1007/BF02245299 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02245299 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Churchill Lynn Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut NATIONALLICENCE 700 1- Austin Mark Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut NATIONALLICENCE 700 1- Kalivas Peter Alcohol and Drug Abuse Program and Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, 99164-6520, Pullman, WA, USA aut NATIONALLICENCE 773 0- Psychopharmacology Springer-Verlag 108/1-2(1992-07-01), 141-146 0033-3158 108:1-2<141 1992 108 213 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer