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chrna3 Modulates Alcohol Response.

Joshua Raine¹, Caroline Kibat^1,2, Tirtha Das Banerjee³

¹Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117593, Singapore.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|September 24, 2025

Summary

This summary is machine-generated.

Nicotinic acetylcholine receptor alpha3 (CHRNA3) influences alcohol response in zebrafish. CHRNA3 dysfunction leads to increased alcohol tolerance and altered social behavior, highlighting its neurogenetic role in alcohol use disorders.

Keywords:

alcohol hormesis nicotine preclinical model substance use disorder zebrafish

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Area of Science:

Neuroscience
Genetics
Pharmacology

Background:

Alcohol use disorders (AUDs) are complex, influenced by multiple factors.
Understanding the neurogenetics of AUDs is crucial for personalized treatments.
Zebrafish offer a valuable model for studying neurobehavioral responses to alcohol.

Purpose of the Study:

To investigate the role of nicotinic acetylcholine receptor subunit alpha3 (CHRNA3) in alcohol self-administration and response.
To explore the neurogenetic underpinnings of alcohol's effects using a zebrafish model.

Main Methods:

Utilized a two-choice self-administration zebrafish assay with juvenile fish.
Examined alcohol's effect on self-administration, shoaling behavior, and locomotion.
Conducted transcriptomic analyses on CHRNA3 mutant zebrafish brains.

Main Results:

Zebrafish exhibit a biphasic, inverted U-shaped alcohol self-administration response.
CHRNA3 mutants show blunted responses to alcohol, including prolonged self-administration and increased gregariousness.
Transcriptomic data indicate alterations in glutamatergic, GABAergic, and cholinergic signaling in CHRNA3 mutants.

Conclusions:

CHRNA3 plays a significant role in regulating alcohol intake and response.
CHRNA3 dysfunction is associated with increased alcohol tolerance and altered neurobehavioral phenotypes.
Zebrafish models provide insights into the neurogenetics of AUDs and potential therapeutic targets.