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Updated: Jul 6, 2025

Assessing Changes in Volatile General Anesthetic Sensitivity of Mice after Local or Systemic Pharmacological Intervention
Published on: October 16, 2013
General Anesthesia Activates a Central Anxiolytic Center in the BNST
Researchers discovered specific neurons in the brain (ovBNST GA) activated by anesthetics and anxiolytics. Activating these neurons reduces anxiety and alters autonomic responses, suggesting a new therapeutic target for anxiety disorders.
Area of Science:
- Neuroscience
- Anesthesiology
- Pharmacology
Background:
- Low doses of anesthetics like ketamine and dexmedetomidine possess anxiolytic effects separate from sedation.
- The precise neural mechanisms underlying these anxiolytic effects remain unclear.
Approach:
- Identified a population of GABAergic neurons in the oval division of the bed nucleus of the stria terminalis (ovBNST GA) activated by anesthetics and diazepam.
- Investigated the role of ovBNST GA neurons, particularly those expressing neurotensin receptor 1 (Ntsr1), in anxiety-related behaviors and autonomic responses using optogenetics.
- Examined the impact of activating or inhibiting these neurons on anxiety-like behaviors in both naive and pain- 모델 mice.
Key Points:
- A majority of ovBNST GA neurons express Ntsr1 and project to brain regions involved in anxiety and stress.
- Optogenetic activation of ovBNST GA /ovBNST Ntsr1 neurons significantly reduced anxiety-like behaviors.
- Inhibition of these neurons increased anxiety-like behaviors.
- Activation of these neurons decreased heart rate and increased heart rate variability, indicating a shift towards an anxiolytic autonomic state.
Conclusions:
- ovBNST GA /ovBNST Ntsr1 neurons represent an endogenous anxiolytic center within the brain.
- These neurons offer a potential therapeutic target for anxiety-related disorders.
- Anesthesia-activated ovBNST neurons bidirectionally modulate anxiety-like behavior and autonomic state.
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