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Related Concept Videos

CNS Depressants: Alcohol and Nicotine01:27

CNS Depressants: Alcohol and Nicotine

887
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...
887

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Related Experiment Video

Updated: Dec 20, 2025

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
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Cortical astrocytes regulate ethanol consumption and intoxication in mice.

E K Erickson1,2, A J DaCosta3, S C Mason3

  • 1Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX, 78712-01095, USA. emmaerickson@utexas.edu.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
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Astrocytes in the brain

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Area of Science:

  • Neuroscience
  • Cellular Biology

Background:

  • Astrocytes are crucial for central nervous system function.
  • Astrocyte dysfunction is linked to psychiatric disorders like alcohol use disorder.
  • Their specific role in ethanol's effects remains unclear.

Purpose of the Study:

  • To investigate the role of astrocyte G-protein coupled-receptor (GPCR)-mediated calcium signaling in ethanol's behavioral effects.
  • To test if modulating astrocyte calcium signaling impacts ethanol consumption and intoxication.

Main Methods:

  • Used astrocyte-specific excitatory DREADDs in the prefrontal cortex (PFC) of mice.
  • Manipulated astrocyte calcium signaling via Gq-GPCR activation and calcium extrusion.
  • Assessed effects on ethanol intake, locomotor activity, and sedative-hypnotic responses.

Main Results:

  • Activating PFC astrocyte Gq-GPCR signaling increased ethanol drinking in naive mice.
  • Reducing astrocyte calcium signaling decreased ethanol intake.
  • Modulated ethanol's stimulant and sedative effects, with adenosine A1 receptors involvement.

Conclusions:

  • PFC astrocytes play a significant role in the behavioral effects of ethanol.
  • Astrocyte calcium signaling, partly via adenosine receptors, influences ethanol consumption and intoxication.