Reinstatement of methamphetamine conditioned place preference in nicotine-sensitized rats

• Published in: Behavioural brain research 2012-12, Vol.235 (2), p.158-165
• Main Authors: Berry, Jennifer N., Neugebauer, Nichole M., Bardo, Michael T.
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Central Nervous System Sensitization - drug effects; Central Nervous System Stimulants - pharmacology; Conditioned place preference; Conditioning, Operant - drug effects; Dose-response effects; Dose-Response Relationship, Drug; Drug Interactions; Drug self-administration; Extinction; Methamphetamine; Methamphetamine - pharmacology; Nicotine; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; Place preferences; Rats; Rats, Sprague-Dawley; Reinforcement; Reinstatement; Reward; Time Factors
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2012.07.043

► Reinstatement of methamphetamine-induced CPP varies as a function of dose. ► Prior exposure to nicotine did not alter methamphetamine-induced CPP. ► Nicotine given in combination with methamphetamine reinstated the preference. ► Nicotine may alter the rewarding effects of methamphetamine. The current experiments examined the effects of repeated nicotine prior to acquisition, extinction, and reinstatement of methamphetamine-induced conditioned place preference (CPP). Methamphetamine-induced (METH; 0.25, 0.5, or 1mg/kg, s.c.) CPP was established using separate groups of adult male Sprague-Dawley rats with an unbiased conditioning procedure. Following extinction of METH CPP, drug-primed reinstatement (0, 0.25, 0.5 or 1mg/kg, s.c.) of METH CPP was assessed in order to determine whether METH-induced reinstatement depends on the METH dose used to induce CPP. In a second experiment, separate groups of rats received nicotine (NIC; 0 or 0.2mg/kg, s.c.) for 7 days prior to undergoing METH (0 or 0.5mg/kg, s.c.) conditioning, extinction, and drug-primed reinstatement. Results indicate that METH-primed reinstatement varied as a function of dose such that priming with the conditioning dose did not reinstate CPP, but reinstatement was observed following priming doses of METH that were either lower or higher than the conditioning dose. Prior NIC exposure had no effect on METH CPP, extinction, or reinstatement. Interestingly, at a METH dose (0.5mg/kg) that did not induce reinstatement alone, acute NIC (0.2mg/kg) in combination with METH induced reinstatement, suggesting that NIC produced a leftward shift in the dose-response effect of METH to reinstate CPP. These studies indicate that prior NIC exposure may not be necessary for enhancement of the rewarding effects of METH, in contrast to previous self-administration reports.