ArticleCommunications biology2024
An ultra-short-acting benzodiazepine in thalamic nucleus reuniens undermines fear extinction via intermediation of hippocamposeptal circuits.
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 7 papers.
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Who cites it
7 citing papers in PubMed.
- Effects of Remimazolam Dose and Bolus Injection Rate on Hiccups During Painless Colonoscopy: A Double-Blind Randomized Clinical Trial.Drug design, development and therapy · 2026Trial
- Comparative effects of remimazolam and propofol on hemodynamic stability during sedation for painless gastroscopy: a randomized clinical trial.BMC anesthesiology · 2025Trial
- Circuit-informed modulation of traumatic memory in PTSD: integrating extinction, suppression, and reconsolidation.Molecular psychiatry · 2026Review
- The thalamic nucleus reuniens orchestrates prefrontal-hippocampal synchrony in memory, emotion, and disease.Frontiers in behavioral neuroscience · 2026Review
- From Bench to Bedside: Understanding General Anesthetics' Impact on PTSD.Current neuropharmacology · 2026Review
- Sleep need-dependent plasticity of a thalamic circuit promotes homeostatic recovery sleep.Science (New York, N.Y.) · 2025Article
- First evidence of an anxiety-like behavior and its pharmacological modulation in a molluscan model organism, Lymnaea stagnalis.Translational psychiatry · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Benzodiazepines, commonly used for anxiolytics, hinder conditioned fear extinction, and the underlying circuit mechanisms are unclear. Utilizing remimazolam, an ultra-short-acting benzodiazepine, here we reveal its impact on the thalamic nucleus reuniens (RE) and interconnected hippocamposeptal circuits during fear extinction. Systemic or RE-specific administration of remimazolam impedes fear extinction by reducing RE activation through A type GABA receptors. Remimazolam enhances long-range GABAergic inhibition from lateral septum (LS) to RE, underlying the compromised fear extinction. RE projects to ventral hippocampus (vHPC), which in turn sends projections characterized by feed-forward inhibition to the GABAergic neurons of the LS. This is coupled with long-range GABAergic projections from the LS to RE, collectively constituting an overall positive feedback circuit construct that promotes fear extinction. RE-specific remimazolam negates the facilitation of fear extinction by disrupting this circuit. Thus, remimazolam in RE disrupts fear extinction caused by hippocamposeptal intermediation, offering mechanistic insights for the dilemma of combining anxiolytics with extinction-based exposure therapy.
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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.