ArticleCommunications biology2024
Neuronal excitation-inhibition imbalance in the basolateral amygdala is involved in propofol-mediated enhancement of fear memory.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Anesthetics as emerging therapeutics for post-traumatic stress disorder (PTSD): bridging bench and bedside.Molecular psychiatry · 2026Review
- From classic circuits to novel mechanisms: How lncRNA, neuroinflammation, and iPSC models address the translational crisis in PTSD research.Comprehensive psychoneuroendocrinology · 2026Review
- A Non-Mitophagy Activity of BNIP3L/NIX in Amygdala Glutamatergic Neurons is Essential for Contextual Fear Memory Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Therapeutic Values of General Anesthetics: From Developmental Neurotoxicity to Neurotherapeutic Agents.Current neuropharmacology · 2026Review
- Exendin-4 enhances GLP-1 signaling and reduces anxiety-like behaviors in male heroin withdrawal mice.PloS one · 2026Article
- The Involvement of the Endocannabinoid, Glutamatergic, and GABAergic Systems in PTSD.International journal of molecular sciences · 2025Review
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Authors and funding
13 authors.
Funding
Abstract
Posttraumatic stress disorder (PTSD) is associated with glutamatergic neuron hyperactivation in the basolateral amygdala (BLA) brain area, while GABAergic interneurons in the BLA modulate glutamatergic neuron excitability. Studies have shown that propofol exerts its effects through potentiation of the inhibitory neurotransmitter γ-aminobutyric acid. The neuronal mechanism by which propofol anesthesia modulates fear memory is currently unknown. Here, we used optogenetics and chemogenetics to suppress glutamatergic neurons or activate GABAergic interneurons in the BLA to assess alterations in neuronal excitation-inhibition balance and investigate fear memory. The excitability of glutamatergic neurons in the BLA was significantly reduced by the suppression of glutamatergic neurons or activation of GABAergic interneurons, while propofol-mediated enhancement of fear memory was attenuated. We suggest that propofol anesthesia could reduce the excitability of GABAergic neurons through activation of GABAA receptors, subsequently increasing the excitability of glutamatergic neurons in the mice BLA; the effect of propofol on enhancing mice fear memory might be mediated by strengthening glutamatergic neuronal excitability and decreasing the excitability of GABAergic neurons in the BLA; neuronal excitation-inhibition imbalance in the BLA might be important in mediating the enhancement of fear memory induced by propofol.
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