Nicotinic receptors and lurasidone-mediated reversal of phencyclidine-induced deficit in novel object recognition

• Published in: Behavioural brain research Vol. 301; pp. 204 - 212
• Main Authors: Miyauchi, Masanori, Neugebauer‎, Nichole M., Oyamada, Yoshihiro, Meltzer, Herbert Y.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.03.2016
• Subjects: Acetylcholine; alpha7 Nicotinic Acetylcholine Receptor - metabolism; Animals; Atypical antipsychotic drug; Azetidines - pharmacology; Benzamides - pharmacology; Bridged Bicyclo Compounds - pharmacology; Cognition Disorders - drug therapy; Cognition Disorders - metabolism; Disease Models, Animal; Female; Lurasidone Hydrochloride - pharmacology; Mecamylamine - pharmacology; Nicotinic acetylcholine receptors; Nicotinic Agonists - pharmacology; Nicotinic Antagonists - pharmacology; Nootropic Agents - pharmacology; Novel object recognition; Phencyclidine; Random Allocation; Rats, Long-Evans; Receptors, Nicotinic - metabolism; MLA; DI; DMSO; ACh; CIAS; AAPD; PFC; Glu; NAc; Atypical antipsychotic drug; Phencyclidine; ANOVA; nAChR; Nicotinic acetylcholine receptors; AChE; ip; MEC; HIP; NOR; mPFC; SED; DHβE; LE; NMDAR; SEM; Acetylcholine; Novel object recognition; PCP; 5-HT; DA; ITI

•Mecamylamine, a non-selective nAChR antagonist, induced a NOR deficit in normal rats.•A-85380, a selective α4β2* nAChR agonist, reversed PCP-induced NOR deficit.•PNU-282987, a selective α7 nAChR agonist, reversed PCP-induced NOR deficit.•The reversal effect of lurasidone was blocked by mecamylamine...