|  Help  |  About  |  Contact Us

Publication : Lack of β2-AR Increases Anxiety-Like Behaviors and Rewarding Properties of Cocaine.

First Author  Zhu H Year  2017
Journal  Front Behav Neurosci Volume  11
Pages  49 PubMed ID  28348522
Mgi Jnum  J:275864 Mgi Id  MGI:6307143
Doi  10.3389/fnbeh.2017.00049 Citation  Zhu H, et al. (2017) Lack of beta2-AR Increases Anxiety-Like Behaviors and Rewarding Properties of Cocaine. Front Behav Neurosci 11:49
abstractText  It is well known that beta-adrenoceptors (beta-ARs) play a critical role in emotional arousal and stressful events, but the specific contributions of the beta2-AR subtype to the psychological disorders are largely unknown. To investigate whether beta2-AR are involved in anxiety-like behavior and reward to addictive drugs, we conducted a series of behavioral tests on beta2-AR knock-out (KO) mice. beta2-AR KO mice exhibited increased preference for the dark compartment and closed arm in tests of Light/Dark box and elevated plus maze, indicating that beta2-AR deletion elevates level of anxiety or innate fear. beta2-AR KO mice also showed decreased immobility in tail suspension test (TST), suggesting that beta2-AR deletion inhibits depression-like behavior. Interestingly, beta2-AR ablation did not change basal locomotion but significantly increased locomotor activity induced by acute cocaine administration. beta2-AR KO mice showed enhanced place preference for cocaine, which could be attenuated by beta1-selective AR antagonist betaxolol. Consistently, beta2-AR agonist suppressed cocaine-conditioned place preference (CPP). These data indicate that beta2-AR deletion enhances acute response and reward to cocaine. Our results suggest that beta2-AR regulates anxiety level, depression-like behavior and hedonic properties of cocaine, implicating that beta2-AR are the potential targets for the treatment of emotional disorders and cocaine addiction.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

7 Authors

1 Bio Entities

Trail: Publication

0 Expression