Modulatory effects of the basolateral amygdala α2-adrenoceptors on nicotine-induced anxiogenic-like behaviours of rats in the elevated plus maze. (June 2016)

• Record Type: Journal Article
• Authors: Bashiri, Hamideh; Rezayof, Ameneh; Sahebgharani, Mousa; Tavangar, Seyed Mohammad; Zarrindast, Mohammad-Reza
• Is Part Of: Neuropharmacology. Volume 105(2016)
• Page Start: 478
• Page End: 486
• Publication Date: 2016-06
• Subjects: Nicotine -- Clonidine -- Yohimbine -- Basolateral amygdala -- Anxiety-like behaviours -- Rat(s); α2-ARs α2-Adrenergic receptors -- ANOVA Analysis of variance -- BLA Basolateral amygdala -- cAMP Cyclic adenosine monophosphate -- CNS Central nervous system -- EPM Elevated plus maze -- GPCRs G-protein-coupled receptors -- LC locus coeruleus -- nAChRs Nicotinic acetylcholine receptors -- NE Norepinephrine -- %OAE Percentage of open arm entries -- %OAT Percentage of open arm time -- SEM Standard error of mean -- WHO World Health Organization; Neuropsychopharmacology -- Periodicals; Autonomic Agents -- Periodicals; Neuropsychopharmacologie -- Périodiques; Neuropsychopharmacology; Periodicals; Electronic journals; 615.78
• DOI: 10.1016/j.neuropharm.2016.02.010
• Languages: English
• ISSNs: 0028-3908

Abstract

Abstract: The present study was designed to clarify whether α2 -adrenoceptors of the basolateral amygdala (BLA) are involved in nicotine-induced anxiogenic-like behaviours. Adult male Wistar rats were bilaterally cannulated in the BLA and anxiety-like behaviours were assessed in an elevated plus maze (EPM) task. Systemic intraperitoneal (i.p.) administration of nicotine (0.3, 0.5 and 0.7 mg/kg) dose-dependently decreased open arm time (%OAT) and open arm entry (%OAE), indicating the anxiogenic-like effect of nicotine. The activation of the BLA α2 -adrenoceptors by the injection of α2 -receptor agonist, clonidine (0.1, 0.3 and 0.5 μg/rat) into the BLA (intra-BLA) reversed nicotine-induced anxiogenic-like behaviours. It is important to note that intra-BLA injection of a higher dose of clonidine (0.5 μg/rat) by itself increased %OAT, but not %OAE which showed an anxiolytic effect of the agonist. On the other hand, intra-BLA injection of different doses of α2 -adrenoceptor antagonist, yohimbine (1, 3 and 5 μg/rat) in combination with an ineffective dose of nicotine (0.3 mg/kg) decreased %OAT and %OAE, suggesting a potentiative effect of the antagonist on nicotine response. In addition, intra-BLA injection of the same doses of yohimbine did not alter %OAT and %OAE. Interestingly, intra-BLA injection of yohimbine (0.5 and 1 μg/rat) significantly reversed the inhibitory effect of clonidine on nicotine-induced anxiogenic-like behaviours. It should be considered that the drug treatments had no effect on locomotor activity in all experiments. Taken together, it can be concluded that nicotine produces anxiogenic-like behaviours which may be mediated through the BLA α2 -adrenoceptor mechanism. Graphical abstract: Highlights: Intraperitoneal injection of nicotine produced anxiety-like behaviours. Intra-BLA injection of clonidine reversed the anxiogenic-like behaviours of nicotine. Intra-BLA injection of yohimbine potentiated nicotine response. Blockade of α2 -ARs reversed the inhibitory effect of clonidine on nicotine response.