Research PapersOrphanin FQ/nociceptin but not Ro 65-6570 inhibits the expression of cocaine-induced conditioned place preferenceKotlińska, J.a; Wichmann, J.b; Legowska, A.c; Rolka, K.c; Silberring, J.dAuthor Information aDepartment of Pharmacodynamics, Medical Academy, 20-081 Lublin, Poland bPharma Division, PRBC-M, F. Hoffmann-La Roche Ltd., Basel, Switzerland cFaculty of Chemistry, University of Gdansk, 80-952 Gdansk, Poland dFaculty of Chemistry, Jagiellonian University, Kraków, Poland Correspondence to Dr Jolanta Kotlińska, Department of Pharmacodynamics, Medical Academy, Staszica 4, 20-081 Lublin, Poland. E-mail: [email protected] Received 7 December 2001 accepted as revised 6 May 2002 Behavioural Pharmacology: May 2002 - Volume 13 - Issue 3 - p 229-235 Buy Abstract The present study investigated the effect of orphanin FQ/nociceptin (OFQ/N), the endogenous ligand of the opioid receptor-like 1 (ORL-1) receptor on the expression of cocaine-induced conditioned place preference (CPP) in rats. To extend this study, the new non-peptidic compound Ro 65-6570 (8-acenaphthen-1-yl-1-phenyl-1,3,8-triaza-spiro[4,5]decan-4-one), with agonist activity at ORL-1 receptors, was examined. The influence of both compounds on cocaine-induced hyperactivity was also studied. Our experiments indicated that intracerebroventricular (i.c.v.) injection of OFQ/N, at doses of 10 and 20 μ g/rat, significantly suppressed the expression of cocaine-induced place preference. Ro 65-6570 (3 and 6 mg/kg, i.p.) did not change the effect of cocaine, although its acute injection in control rats significantly increased the time spent in the drug-associated compartment of the CPP apparatus. The substances exhibited opposite effects on cocaine-induced hyperactivity (OFQ/N suppressed it but Ro 65-6570 increased it). Our results suggest that the effect of OFQ/N on the expression of cocaine-induced CPP may be a result of its influence on dopamine (DA) neurotransmission in mesolimbic structures. Ro 65-6570 does not share this effect with OFQ/N. © 2002 Lippincott Williams & Wilkins, Inc.