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首页> 外文期刊>The European Journal of Neuroscience >Intermittent ethanol exposure induces inflammatory brain damage and causes long-term behavioural alterations in adolescent rats.
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Intermittent ethanol exposure induces inflammatory brain damage and causes long-term behavioural alterations in adolescent rats.

机译：间歇性乙醇暴露会诱发脑炎性损伤，并引起青春期大鼠的长期行为改变。

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摘要

Adolescent brain development seems to be important for the maturation of brain structures and behaviour. Intermittent binge ethanol drinking is common among adolescents, and this type of drinking can induce brain damage. Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol intoxication enhances cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions. Adolescent rats were exposed to ethanol (3.0 g/kg) for two consecutive days at 48-h intervals over 14 days. Levels of COX-2, iNOS and cell death were assessed in the neocortex, hippocampus and cerebellum 24 h after the final ethanol administration. The following day or 20 days after the final injection (adult stage), animals were tested for different behavioural tests (conditional discrimination learning, rotarod, object recognition, beam-walking performance) to assess cognitive and motor functions. Our results show that intermittent ethanol intoxication upregulates COX-2 and iNOS levels, and increases cell death in the neocortex, hippocampus and cerebellum. Furthermore, animals treated with ethanol during adolescence exhibited behavioural deficits that were evident at the end of ethanol treatments and at the adult stage. Administration of indomethacin, a COX-2 inhibitor, abolishes the induction of COX-2 and iNOS expression and cell death, preventing ethanol-induced behavioural deficits. These findings indicate that binge pattern exposure to ethanol during adolescence induces brain damage by inflammatory processes and causes long-lasting neurobehavioural consequences. Accordingly, administering indomethacin protects against ethanol-induced brain damage and prevents detrimental ethanol effects on cognitive and motor processes.
机译：青春期的大脑发育对于大脑结构和行为的成熟似乎很重要。间歇性酗酒在青少年中很常见，这种类型的饮酒会诱发脑损伤。因为我们已经证明了慢性乙醇治疗会诱导大脑中的炎症过程，所以我们研究了间歇性乙醇中毒是否会增强青春期大鼠的环氧合酶2（COX-2）和可诱导性一氧化氮合酶（iNOS），以及这些介体是否会诱发脑损伤和引起永久性认知功能障碍。青春期大鼠在14天内连续48天间隔两天暴露于乙醇（3.0 g / kg）。在最后一次乙醇给药后24小时，在新皮层，海马和小脑中评估了COX-2，iNOS和细胞死亡的水平。在最后一次注射（成人阶段）后的第二天或第二十天，对动物进行不同的行为测试（条件判别学习，旋转脚架，物体识别，电子束行走性能）以评估认知和运动功能。我们的结果表明，间歇性乙醇中毒会上调COX-2和iNOS的水平，并增加新皮层，海马和小脑的细胞死亡。此外，在青春期期间接受乙醇治疗的动物表现出行为缺陷，这在乙醇治疗结束时和成年阶段均很明显。施用吲哚美辛（一种COX-2抑制剂）可消除对COX-2和iNOS表达的诱导以及细胞死亡，从而防止乙醇引起的行为缺陷。这些发现表明，青春期暴饮暴食的乙醇暴露会通过炎症过程引起脑损伤，并引起长期的神经行为后果。因此，施用消炎痛可防止乙醇引起的脑损伤并防止乙醇对认知和运动过程的有害影响。

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