Chronic restraint stress and acute binge ethanol intoxication induce apoptosis in the adolescent brain.

FERNANDEZ M.; DE OLMOS, S; FERREYRA, A.; PAUTASSI R.M.

Puerto Varas

Congreso; VIII LASBRA International meeting: Neurobiological basis of alcoholism: from molecules to behavior; 2017

Latin American Society for Biomedical Research on Alcoholism

Restraint stress (RS) promotes release of corticosteroids and induces neurotoxicity in the hippocampus. Most of the studies analyzing this phenomenon have employed protracted (i.e., ≈ 21 days) exposure to restraint stress. RS also increases ethanol intake and exacerbates anxiety patterns in adolescent and adult rats, an effect that is reversed by ethanol administration only in adolescents. Binge ethanol administration can induce brain toxicity, analogous to that induced by stress. On the basis of this, it could be postulated that ethanol intoxication may facilitate stress-induced neurotoxicity. In the present study, we analyzed whether adolescent rats exposed to five episodes of RS exhibit neurodegeneration in the dorsal and ventral hippocampus[CA1, CA2, CA3 and dentate gyrus (DG)]; and whether this is modulated by a binge, yet brief (two administrations of 2.5 g/kg ethanol, separated by 120 min), ethanol administration. The results indicated a synergistic, neurotoxic effect between RS and ethanol in dorsal DG; whereas RS induced neurodegeneration in CA1 of dorsal hippocampus and CA2 and CA3 of ventral hippocampus. Binge ethanol administration induced neurotoxic effects in DG and CA2 and CA3 of dorsal hippocampus and in CA1,CA2 and CA3 of ventral hippocampus. The study highlights the vulnerability of the developing brain to alcohol insult and stress exposure.