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Related Concept Videos

CNS Depressants: Alcohol and Nicotine01:27

CNS Depressants: Alcohol and Nicotine

185
Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
185

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Updated: Jun 16, 2025

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
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Integrated Single-Cell Multiomic Profiling of Caudate Nucleus Suggests Key Mechanisms in Alcohol Use Disorder.

Nick Green1, Hongyu Gao1,2, Xiaona Chu1

  • 1Indiana University School of Medicine, Department of Medical and Molecular Genetics, Indianapolis, Indiana 46202, United States.

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Alcohol use disorder (AUD) causes significant gene expression changes in the brain

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Area of Science:

  • Neuroscience and Genetics
  • Molecular Biology
  • Addiction Research

Background:

  • Alcohol use disorder (AUD) involves complex brain changes, particularly in the understudied caudate nucleus.
  • Understanding cell-type-specific molecular alterations is crucial for AUD research.

Purpose of the Study:

  • To investigate the transcriptional and regulatory changes in the caudate nucleus associated with AUD.
  • To identify cell types and molecular pathways involved in AUD pathogenesis using multiomic approaches.

Main Methods:

  • Paired single-nucleus RNA sequencing (snRNA-seq) and ATAC sequencing (snATAC-seq) on 143 human postmortem caudate samples (74 with AUD).
  • Identification of 17 distinct cell types and analysis of gene expression and chromatin accessibility alterations.
  • Cell type-specific expression quantitative trait loci (eQTL) analysis integrated with GWAS data.

Main Results:

  • Significant alcohol-induced gene expression changes were linked to altered chromatin accessibility across multiple cell types.
  • Medium spiny neurons showed novel differences impacting RNA metabolism and immune response pathways.
  • Microglia displayed unique activation states, reactive astrocytes influenced glutamatergic pathways, and oligodendrocytes showed dysregulation linked to demyelination and altered signaling.

Conclusions:

  • AUD involves widespread cell-type-specific molecular dysregulation in the caudate nucleus, mediated by chromatin accessibility.
  • Identified novel AUD risk genes (e.g., ADAL, PPP2R3C) by linking genetic variants to gene expression and chromatin accessibility.
  • Demonstrates the power of large-scale multiomic studies for understanding complex gene regulation in neurological disorders.