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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

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Persisting changes in basolateral amygdala mRNAs after chronic ethanol consumption.

A M Falco¹, H C Bergstrom, S E Bachus

¹George Mason University, Fairfax, VA 22030, USA. afalco@gmu.edu

Physiology & Behavior

|October 22, 2008

Summary

Adolescent alcohol use can increase the risk of dependence. Chronic ethanol consumption in adulthood, but not adolescence, altered neurochemistry in the basolateral amygdala in rats.

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Area of Science:

Neuroscience
Neurobiology
Addiction Research

Background:

Adolescent alcohol consumption is prevalent and linked to higher risks of future alcohol dependence.
Chronic alcohol use can cause lasting changes in the amygdala, potentially worsening negative emotions and increasing alcohol intake.

Purpose of the Study:

To investigate the long-term effects of ethanol consumption on basolateral amygdala mRNA levels.
To compare the impact of adolescent versus adult ethanol exposure on neurochemistry.

Main Methods:

Rats were given restricted access to ethanol during adolescence or adulthood.
Following a 60-day abstinence period, brain tissue was analyzed using in situ hybridization.
Specific mRNAs (GABA(A) alpha(1), GAD(67), CRF, NMDA NR2A) in the basolateral amygdala were quantified.

Main Results:

Adult ethanol consumers showed decreased GABA(A) alpha(1), GAD(67), and CRF mRNAs compared to controls.
No significant mRNA changes were observed in adolescent ethanol consumers.
Changes were specific to the basolateral amygdala, not the piriform cortex.

Conclusions:

Chronic ethanol consumption leads to age-dependent neurochemical alterations in the rat basolateral amygdala.
Adult-onset ethanol use has a more significant impact on amygdala gene expression than adolescent-onset use.