Binge-like ethanol induced anxiety- like behavior, cell degeneration and possible amelioration of Omega-3 (ω-3) Fatty Acids in adolescent rats

Abstract

Alcohol consumption contributes to ∼5% of the global disease burden, with adolescents being particularly vulnerable. High alcohol exposure induces anxiety-like behavior and neuronal death, potentially through neuroinflammation and oxidative stress–induced apoptosis. Omega-3 (ω-3) fatty acids may counteract these effects through their anti-inflammatory and antioxidant properties. However, little is known about the long-term effects of ethanol (EtOH) exposure and the potential protective ω-3 effects in adolescents. Here, we evaluated the impact of EtOH exposure and the neuroprotective role of ω-3 on anxiety-like behavior and pyknotic cell number, in adolescent rats. Animals received 2 or 0 g/kg of EtOH (ig) on postnatal days (PDs) 28, 30, and 32 and, fifteen min later, they were administered with ω-3 (720 or 0 mg/kg, ig). On PD 34, animals were tested in the elevated plus maze for 5 min and were sacrificed for brain tissue collection. Pyknotic cells were stained with toluidine blue and quantified in the central amygdala (CeA). EtOH-treated animals showed an anxiogenic profile, spending less time in open arms; a profile that was improved by ω-3 (EtOH+ω-3 animals increase the time in open arms). EtOH significantly increased the pyknotic cell number in the CeA. These findings highlight ethanol´s long-term neurotoxic effects on cell degeneration and anxiety and provide evidence of possible amelioration of ω-3 in adolescents.