ArticleInternational journal of molecular sciences2022
β2-Adrenoceptors in the Medial Prefrontal Cortex Excitatory Neurons Regulate Anxiety-like Behavior in Mice.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Biased signaling of β2-adrenergic receptor in physiological and pathological states.Cellular & molecular biology letters · 2026Review
- Recent Developments in the Optical Control of Adrenergic Signaling.Medicinal research reviews · 2025Review
- Prelimbic Cortex Activity Predicts Anxiety-Like Behavior in the Elevated Plus Maze.The European journal of neuroscience · 2025Article
- Minocycline AmelioratesBrain sciences · 2025Article
- Optical Approaches for Investigating Neuromodulation and G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2023Review
- Prefrontal modulation of anxiety through a lens of noradrenergic signaling.Frontiers in systems neuroscience · 2023Review
- Noradrenergic signaling mediates cortical early tagging and storage of remote memory.Nature communications · 2022Article
- Neuro-Plastic Mechanisms of Pain and Addiction.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.