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<p>Excessive alcohol drinking can induce seizures, but the mechanisms underlying acute alcohol-induced seizures remained to be extensively investigated. To investigate this, we established an acute alcohol-treated model and observed a microglial response in the hippocampal CA1 region of mice, which was associated with the enhancement of seizure susceptibility. Furthermore, we found an increased abundance of GABAergic interneurons and a decrease in the activity of CaMKII in the hippocampal CA1 region. Minocycline-mediated microglial depletion fully inhibited the increase in GABAergic interneurons and GABAergic inhibitory synapse formation, and the decrease in glutamatergic neurons and glutamatergic excitatory synapse formation induced by acute alcohol treatment. In conclusion, our findings indicate that dysregulation of synapse formation via microglial activation contributes to acute alcohol-induced enhancement of seizure susceptibility.</p>

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Microglial activation drives neuronal dysregulation in alcohol-induced seizure susceptibility

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月3日

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  • Shiyong Zhang,
  • Yuting Zhou,
  • Yue Ren,
  • Juntong Shang,
  • Ao Jiang,
  • Yiming Hong,
  • Shennuoxue Hong,
  • Congcong Wang,
  • Wenjuan Wang,
  • Juan Chen

摘要

Excessive alcohol drinking can induce seizures, but the mechanisms underlying acute alcohol-induced seizures remained to be extensively investigated. To investigate this, we established an acute alcohol-treated model and observed a microglial response in the hippocampal CA1 region of mice, which was associated with the enhancement of seizure susceptibility. Furthermore, we found an increased abundance of GABAergic interneurons and a decrease in the activity of CaMKII in the hippocampal CA1 region. Minocycline-mediated microglial depletion fully inhibited the increase in GABAergic interneurons and GABAergic inhibitory synapse formation, and the decrease in glutamatergic neurons and glutamatergic excitatory synapse formation induced by acute alcohol treatment. In conclusion, our findings indicate that dysregulation of synapse formation via microglial activation contributes to acute alcohol-induced enhancement of seizure susceptibility.