ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016
Fluoxetine Facilitates Fear Extinction Through Amygdala Endocannabinoids.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- The effect of SSRIs on fear learning: a systematic review and meta-analysis.Psychopharmacology · 2023Pooled it
- Article
- Parietal-Frontal Pathway Controls Relapse of Fear Memory in a Novel Context.Biological psychiatry global open science · 2024Article
- REM disruption and REM Vagal Activity Predict Extinction Recall in Trauma-Exposed Individuals.bioRxiv : the preprint server for biology · 2024Article
- Effects of cannabidiol on fear conditioning in anxiety disorders: decreased threat expectation during retention, but no enhanced fear re-extinction.Psychopharmacology · 2024Article
- Post-traumatic stress disorder: the role of the amygdala and potential therapeutic interventions - a review.Frontiers in psychiatry · 2024Review
- Article
- Alleviating anxiety and taming trauma: Novel pharmacotherapeutics for anxiety disorders and posttraumatic stress disorder.Neuropharmacology · 2023Review
- Enhancing Psychological Interventions for Post-Traumatic Stress Disorder (PTSD) Treatment with Memory Influencing Drugs.Current neuropharmacology · 2023Review
- Fatty acid amide hydrolase inhibition and N-arachidonoylethanolamine modulation by isoflavonoids: A novel target for upcoming antidepressants.Pharmacology research & perspectives · 2022Article
- Perinatal CBD or THC Exposure Results in Lasting Resistance to Fluoxetine in the Forced Swim Test: Reversal by Fatty Acid Amide Hydrolase Inhibition.Cannabis and cannabinoid research · 2022Article
- Local modulation by presynaptic receptors controls neuronal communication and behaviour.Nature reviews. Neuroscience · 2022Review
- Targeting the Endocannabinoid System in the Treatment of Posttraumatic Stress Disorder: A Promising Case of Preclinical-Clinical Translation?Biological psychiatry · 2022Review
- The endocannabinoid system in the amygdala and modulation of fear.Progress in neuro-psychopharmacology & biological psychiatry · 2021Review
- Cessation of fluoxetine treatment increases alcohol seeking during relapse and dysregulates endocannabinoid and glutamatergic signaling in the central amygdala.Addiction biology · 2020Article
- Clinical Therapeutic Strategy and Neuronal Mechanism Underlying Post-Traumatic Stress Disorder (PTSD).International journal of molecular sciences · 2019Review
- Threat-related disorders as persistent motivational states of defense.Current opinion in behavioral sciences · 2019Article
- Additive effect of 5-HT2C and CB1 receptor blockade on the regulation of sleep-wake cycle.BMC neuroscience · 2019Article
- Upregulation of Anandamide Hydrolysis in the Basolateral Complex of Amygdala Reduces Fear Memory Expression and Indices of Stress and Anxiety.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Rodent models of impaired fear extinction.Psychopharmacology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Pharmacologically elevating brain endocannabinoids (eCBs) share anxiolytic and fear extinction-facilitating properties with classical therapeutics, including the selective serotonin reuptake inhibitor, fluoxetine. There are also known functional interactions between the eCB and serotonin systems and preliminary evidence that antidepressants cause alterations in brain eCBs. However, the potential role of eCBs in mediating the facilitatory effects of fluoxetine on fear extinction has not been established. Here, to test for a possible mechanistic contribution of eCBs to fluoxetine's proextinction effects, we integrated biochemical, electrophysiological, pharmacological, and behavioral techniques, using the extinction-impaired 129S1/Sv1mJ mouse strain. Chronic fluoxetine treatment produced a significant and selective increase in levels of anandamide in the BLA, and an associated decrease in activity of the anandamide-catabolizing enzyme, fatty acid amide hydrolase. Slice electrophysiological recordings showed that fluoxetine-induced increases in anandamide were associated with the amplification of eCB-mediated tonic constraint of inhibitory, but not excitatory, transmission in the BLA. Behaviorally, chronic fluoxetine facilitated extinction retrieval in a manner that was prevented by systemic or BLA-specific blockade of CB1 receptors. In contrast to fluoxetine, citalopram treatment did not increase BLA eCBs or facilitate extinction. Taken together, these findings reveal a novel, obligatory role for amygdala eCBs in the proextinction effects of a major pharmacotherapy for trauma- and stressor-related disorders and 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.