Chronic intermittent ethanol administration differentially alters DeltaFosB immunoreactivity in cortical-limbic structures of rats with high and low alcohol preference (2019)

Am J Drug Alcohol Abuse. 2019;45(3):264-275. doi: 10.1080/00952990.2019.1569667.

Wscieklica T1, Le Sueur-Maluf L1, Prearo L2, Conte R3, Viana MB1, Céspedes IC4.



The role of specific cerebral areas involved in alcohol use disorder, such as the amygdala, hippocampus and prefrontal cortex, has emerged as a subject of interest over recent years. Nevertheless, the role played by these regions is frequently confounded by different variables, among them are the patterns of alcohol consumption presented by the subjects.


The present study verified the effects of chronic voluntary ethanol intake (20 sessions) on DeltaFosB immunoreactivity (DeltaFosB-ir) in the amygdala, hippocampus and prefrontal cortex of rats showing high and low preference for ethanol.


DeltaFosB-ir induced by chronic voluntary ethanol intake with a two-bottle intermittent access to 20% ethanol model in male Wistar rats was measured. Three groups of animals were analyzed: control (n = 6), low preference (n = 8) and high preference (n = 8) for ethanol, the latter two categorized from their pattern of voluntary consumption of the alcohol solution.


Ethanol intake in high-preference rats increased DeltaFosB-ir in the central amygdala, CA1 and CA3 regions of the hippocampus and decreased DeltaFosB-ir in the prelimbic cortex and anterior cingulate cortex. On the other hand, in low preference rats, chronic voluntary ethanol intake decreased DeltaFosB-ir in the medial amygdala, basolateral amygdala, dentate gyrus and anterior cingulate cortex.


The present results suggest that different alcohol intake patterns are associated with a specific pattern of DeltaFosB-ir in brain structures that play a key role in controlling behavior and decision making, that is the amygdala, the hippocampus and the prefrontal cortex.

KEYWORDS: Alcohol use disorder; DeltaFosB immunoreactivity; amygdala; chronic intermittent ethanol administration; hippocampus; prefrontal cortex

PMID: 30849242

DOI: 10.1080/00952990.2019.1569667