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.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Bashiri H,Rezayof A,Sahebgharani M,Tavangar SM,Zarrindast MRdoi
10.1016/j.neuropharm.2016.02.010subject
Has Abstractpub_date
2016-06-01 00:00:00pages
478-486eissn
0028-3908issn
1873-7064pii
S0028-3908(16)30045-4journal_volume
105pub_type
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