β2-Adrenoceptors in the Medial Prefrontal Cortex Excitatory Neurons Regulate Anxiety-like Behavior in Mice

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Author(s)

  • Yukyan Lam
  • Cheukhin Li
  • Zhongqi Fu
  • Aruna S. Ramkrishnan

Detail(s)

Original languageEnglish
Article number5578
Journal / PublicationInternational Journal of Molecular Sciences
Volume23
Issue number10
Online published17 May 2022
Publication statusPublished - May 2022

Link(s)

Abstract

The medial prefrontal cortex (mPFC) and β-adrenoceptors (βARs) have been implicated in modulating anxiety-like behavior. However, the specific contributions of the β2-AR subtype in mPFC in anxiety are still unclear. To address this issue, we used optogenetic and microRNA-based (miRNA) silencing to dissect the role of β2-AR in mPFC in anxiety-like behavior. On the one hand, we use a chimeric rhodopsin/β2-AR (Opto-β2-AR) with in vivo optogenetic techniques to selectively activate β2-adrenergic signaling in excitatory neurons of the mPFC. We found that opto-activation of β2-AR is sufficient to induce anxiety-like behavior and reduce social interaction. On the other hand, we utilize the miRNA silencing technique to specifically knock down the β2-AR in mPFC excitatory neurons. We found that the β2-AR knock down induces anxiolytic-like behavior and promotes social interaction compared to the control group. These data suggest that β2-AR signaling in the mPFC has a critical role in anxiety-like states. These findings suggest that inhibiting of β2-AR signaling in the mPFC may be an effective treatment of anxiety disorders.

Research Area(s)

  • norepinephrine, β2-adrenoceptors, optogenetics, neuronal manipulation, microRNA-based silencing, medial prefrontal cortex, excitatory neurons, anxiety, social behavior, anxiolytic therapy, LOCUS-COERULEUS, DECISION-MAKING, STRESS, MEMORY, ACTIVATION, ORGANIZATION, PROPRANOLOL, EXPRESSION, PREVENTS

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