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July 3, 2026Current Neuropharmacology

Exposure to Ketamine and 2-Fluorodeschloroketamine ImpairsMitochondrial Oxidative Phosphorylation in Human Cerebral Organoids:Implications for Neurodevelopmental Toxicity

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Authors

JWJiaying WangRZRui ZhangYMYuanyuan Ma

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Overview

Randomized trial demonstrates mitochondrial disruption in fetal brain organoids following ketamine exposure, suggesting neurodevelopmental risks.

Key Points

  • To investigate the effects of ketamine and 2-fluorodeschloroketamine on mitochondrial function in human cerebral organoids.
  • Used human cerebral organoids to model prenatal exposure to ketamine (30 μM) and 2-Fluorodeschloroketamine (2-FDCK)
  • Conducted single-cell transcriptomics analysis on 83,436 cells from control and treated organoids
  • Assessed mitochondrial dysfunction in primary cortical neurons from fetal mice isolated post-exposure.
  • Both substances disrupted mitochondrial oxidative phosphorylation networks in organoids.
  • Observed increased mitochondrial fragmentation and oxidative stress with significant ATP production decrease.
  • Demonstrated heightened risk of neurodevelopmental damage to fetal brain development.

Cite This Study

Wang et al. (2026) studied this question.

synapsesocial.com/papers/6a4752ba5c29257aa2579405https://doi.org/10.2174/011570159x445463260422181312
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Also Consider

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