Volume 23, Issue 2 (June 2019)                   Physiol Pharmacol 2019, 23(2): 101-114 | Back to browse issues page

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Hosseinmardi L, Shiravi A, Meftahi G H, Afarinesh M R. Inactivation of β1-adrenergic receptor in the basolateral amygdala nucleus attenuated anxiety-like behaviour in response to foot-shock stress in the male rat. Physiol Pharmacol. 2019; 23 (2) :101-114
URL: http://phypha.ir/ppj/article-1-1421-en.html
Abstract:   (498 Views)
Introduction: The basolateral amygdala (BLA) is implicated in stress-related disorders such as anxiety-like behavior. Substantial data exist demonstrating a close relationship between anxiety and adrenergic receptor function in patients with anxiety disorders; however, little is known about the effects of the β1 adrenergic receptor in the BLA on anxiety. This experiment examined the effects of the β1 adrenergic receptor in the BLA on anxiety-like behavior. Methods: Male Wistar rats were exposed to foot-shock stress four consecutive days that were uncontrollable. The β1-adrenoreceptor agonist (dobutamine; 0.5μl/side) or antagonist (atenolol; 0.25μl/side) bilaterally infused into the BLA five minutes before foot-shock stress. Anxiety-like behaviors were assessed 24h after four consecutive day’s uncontrollable stress using elevated plus-maze (EPM) and open field test (OFT). Results: Findings of EPM revealed that foot-shock stress leads to anxiogenic effect with reduction the time spent and the number of entries into the open arms and increased head-dipping. Intra-BLA infusions of atenolol before stress affected animal behavior differently, such that it significantly increased the time spent and the number of entries into the open arms and decreased head-dipping. Also, OFT results showed the intra-BLA infusion of atenolol increased the time periods spent in the center, number of center entries and reduced the number of rearing as compared with the stress group. Conclusion: These results suggest that the anxiety-like behavior observed after the foot-shock stress is mediated, in part, by exaggerated β1 adrenergic receptor acting at the BLA.
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Types of Manuscript: Original Research | Subject: Pharmacology