ArticleBrain and behavior2026
A Single Dose of a Psychedelic Drug Repairs Prefrontal Cortex Synaptic Physiology in a Mouse Model of Prenatal Alcohol Exposure.
Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Psychedelics in Mental Health: Opportunities and Challenges.Brain and behavior · 2026Article
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Authors and funding
3 authors.
Funding
Abstract
backgroundPrenatal alcohol exposure (PAE) can cause fetal alcohol spectrum disorders (FASDs), which are characterized by neural circuit and behavioral dysfunction due to impaired brain development. At the neural and behavioral levels, PAE is associated with disrupted cortical synaptic transmission and lifelong impairments in learning and cognitive control. Despite the prevalence of FASDs (affecting up to one in 20 school-aged children in the United States) and the associated personal, familial, and societal costs, there are currently no treatments to reverse neural circuit dysfunction.
methodsUsing whole-cell patch-clamp electrophysiology, we investigated intrinsic excitability and synaptic activity in prefrontal cortex (PFC) pyramidal neurons from adolescent mice prenatally exposed to ethanol (6.6%) and later given a single injection of either saline or 25CN-NBOH, a psychedelic neuroplastogen.
resultsWe found that PAE reduced intrinsic excitability and synaptic drive in PFC pyramidal neurons. 25CN-NBOH treatment partially rescued intrinsic excitability deficits and restored synaptic drive.
conclusionsPsychedelic neuroplastogens may show promise as potential therapeutics for synaptic deficits associated with PAE and should be further explored in preclinical models.
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