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Microglia depletion and alcohol: Transcriptome and behavioral profiles.

Anna S Warden^1,2, Todd A Triplett^3,4, Aram Lyu³

¹Waggoner Center for Alcoholism and Addiction Research, University of Texas at Austin, Austin, TX, USA.

Addiction Biology

|March 17, 2020

Summary

Microglia do not initiate harmful effects of alcohol abuse. However, microglia depletion blocked alcohol intake escalation following immune activation, suggesting a role in alcohol dependence with sufficient immune stimulation.

Keywords:

PLX5622 alcohol astrocytes microglia neuroimmune transcriptome

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Area of Science:

Neuroscience
Immunology
Alcohol Research

Background:

Alcohol abuse alters microglia, but their role in alcohol-related behaviors is debated.
Understanding microglia's function in alcohol consumption is crucial for developing targeted therapies.

Purpose of the Study:

To investigate the role of microglia in acute and voluntary alcohol consumption behaviors.
To determine if microglia are primary effectors or amplifiers of alcohol's harmful effects.

Main Methods:

Utilized a colony-stimulating factor 1 receptor inhibitor (PLX5622) for microglia depletion.
Assessed effects on acute intoxication, voluntary alcohol consumption, and gene expression.
Employed polyinosinic:polycytidylic acid (poly(I:C)) to induce immune activation and assess microglia's role.

Main Results:

Microglia depletion did not affect acute intoxication or voluntary alcohol consumption.
Transcriptomic analysis revealed compensatory astrocyte gene upregulation.
Microglia depletion blocked alcohol intake escalation following poly(I:C)-induced immune activation.

Conclusions:

Microglia are not the primary regulators of acute and voluntary alcohol behaviors.
Microglia play a regulatory role in alcohol intake escalation when immune activation is sufficient.
Findings provide insight into the causal vs. consequential role of microglia in alcohol use disorder progression.