Facultad de Medicina, Departamento de Toxicología y Farmacología, 1ª Cátedra de Farmacología, Buenos Aires, Universidad de Buenos Aires (UBA), Paraguay 2155, piso 15, 1121, Ciudad Autónoma de Buenos Aires, Argentina.
Instituto de Biología Celular y Neurociencias (IBCN), Universidad de Buenos Aires (UBA)-Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
Neurotox Res. 2024 Jun 10;42(3):29. doi: 10.1007/s12640-024-00707-1.
Ethanol (EtOH) intake and noise exposure are particularly concerning among human adolescents because the potential to harm brain. Unfortunately, putative underlying mechanisms remain to be elucidated. Moreover, implementing non-pharmacological strategies, such as enriched environments (EE), would be pertinent in the field of neuroprotection. This study aims to explore possible underlying triggering mechanism of hippocampus-dependent behaviors in adolescent animals of both sexes following ethanol intake, noise exposure, or a combination of both, as well as the impact of EE. Adolescent Wistar rats of both sexes were subjected to an intermittent voluntary EtOH intake paradigm for one week. A subgroup of animals was exposed to white noise for two hours after the last session of EtOH intake. Some animals of both groups were housed in EE cages. Hippocampal-dependent behavioral assessment and hippocampal oxidative state evaluation were performed. Results show that different hippocampal-dependent behavioral alterations might be induced in animals of both sexes after EtOH intake and sequential noise exposure, that in some cases are sex-specific. Moreover, hippocampal oxidative imbalance seems to be one of the potential underlying mechanisms. Additionally, most behavioral and oxidative alterations were prevented by EE. These findings suggest that two frequently found environmental agents may impact behavior and oxidative pathways in both sexes in an animal model. In addition, EE resulted a partially effective neuroprotective strategy. Therefore, it could be suggested that the implementation of a non-pharmacological approach might also potentially provide neuroprotective advantages against other challenges. Finally, considering its potential for translational human benefit might be worth.
乙醇（EtOH）摄入和噪声暴露在人类青少年中尤其令人担忧，因为它们有可能损害大脑。不幸的是，潜在的机制仍有待阐明。此外，实施非药物策略，如丰富环境（EE），在神经保护领域是相关的。本研究旨在探索青少年动物在乙醇摄入、噪声暴露或两者结合后，以及 EE 对海马依赖行为的潜在潜在触发机制。雄性和雌性 Wistar 大鼠接受了一周的间歇性自愿乙醇摄入范式。一组动物在最后一次乙醇摄入后接受了两小时的白噪声暴露。两组动物的一些动物被安置在 EE 笼中。进行了海马依赖性行为评估和海马氧化状态评估。结果表明，乙醇摄入和序贯噪声暴露后，雄性和雌性动物可能会出现不同的海马依赖性行为改变，在某些情况下是性别特异性的。此外，海马氧化失衡似乎是潜在的潜在机制之一。此外，EE 预防了大多数行为和氧化改变。这些发现表明，两种常见的环境因素可能会在动物模型中对两性的行为和氧化途径产生影响。此外，EE 是一种有效的神经保护策略。因此，可以认为实施非药物方法也可能对其他挑战提供潜在的神经保护优势。最后，考虑到其对人类的潜在益处，可能值得进一步研究。
