• Alcohol;
  • FosB/ΔFosB;
  • Opioid Receptors

Background:  ΔFosB is the best characterized transcription factor induced by chronic stimulation. Although previous studies have demonstrated that chronic passive ethanol exposure alters ΔFosB immunoreactivity (IR), the effect of chronic voluntary ethanol consumption on ΔFosB remains unknown. Furthermore, although previous studies have demonstrated that the opioid antagonist naltrexone reduces alcohol consumption in clinical and preclinical settings, the effect of naltrexone on FosB/ΔFosB has not been explored. Here, we examined the effects of chronic voluntary ethanol intake and naltrexone on FosB/ΔFosB IR in striatal region and prefrontal cortex, and the effect of naltrexone on voluntary ethanol intake.

Methods:  We utilized immunohistochemistry to define the changes in FosB/ΔFosB IR induced by chronic voluntary ethanol intake under a two-bottle intermittent access of 20% ethanol model and by systematic administration (intraperitoneal injection) of naltrexone in Sprague-Dawley rats.

Results:  Chronic (15 drinking sessions in 35 days) voluntary ethanol intake robustly induces FosB/ΔFosB IR in nucleus accumbens core, dorsolateral striatum, and orbitofrontal cortex, but not in nucleus accumbens shell, dorsomedial striatum, and medial prefrontal cortex. Systemic administration of naltrexone for 6 days significantly reduced voluntary ethanol consumption and FosB/ΔFosB IR induced by chronic voluntary ethanol intake.

Conclusion:  Our results suggest that chronic voluntary ethanol intake induces FosB/ΔFosB IR in a subregion-specific manner which involves the activation of endogenous opioid system.