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

FERREYRA ANA; DE OLMOS SOLEDAD ; FERNANDEZ, MACARENA SOLEDAD; PAUTASSI RM

Puerto Varas

Congreso; VIII International meeting of the Latinamerican Society of Research on Alcoholism (LASBRA): ?Neurobiological basis y of alcoholism: from molecules to behavior?.; 2017

LASBRA

Restraint stress (RS) promotes release ofcorticosteroids and induces neurotoxicity inthe hippocampus. Most of the studiesanalyzing this phenomenon have employedprotracted days) exposure to restraint stress.RS also increases ethanol intake andexacerbates anxiety patterns in adolescentand adult rats, an effect that is reversed byethanol administration only in adolescents.Binge ethanol administration can inducebrain toxicity, analogous to that induced bystress. On this basis, it could be postulatedthat ethanol intoxication may facilitate stressinduced neurotoxicity. In the present study,we analyzed whether adolescent rats exposedto five episodes of RS exhibitneurodegeneration in the dorsal and ventralhippocampus [CA1, CA2, CA3 and dentategyrus (DG)]; and whether this is modulated bya binge, yet brief (two administrations of 2.5g/kg ethanol, separated by 120 min), ethanoladministration. The results indicated asynergistic, neurotoxic effect between RS andethanol in dorsal DG; whereas RS inducedneurodegeneration in CA1 of dorsalhippocampus and CA2 and CA3 of ventralhippocampus. Binge ethanol administrationinduced neurotoxic effects in DG and CA2and CA3 of dorsal hippocampus and in CA1,CA2 and CA3 of ventral hippocampus. Thestudy highlights the vulnerability of thedeveloping brain to alcohol insult and stressexposure.