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首页> 外文期刊>Alcohol >MK-801 administration during neonatal ethanol withdrawal attenuates interpositus cell loss and juvenile eyeblink conditioning deficits.
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MK-801 administration during neonatal ethanol withdrawal attenuates interpositus cell loss and juvenile eyeblink conditioning deficits.

机译：新生儿戒断乙醇期间进行MK-801给药可减轻间质细胞损失和青少年眨眼条件障碍。

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Binge-level doses of ethanol have been demonstrated to severely disrupt the cerebellum and cerebellum-dependent tasks when administered to rodent subjects during the early postnatal period. N-methyl-d-aspartic acid (NMDA) receptor-mediated excitotoxicity associated with ethanol withdrawal has been implicated as a significant component contributing to neurotoxic effects resulting from early ethanol exposure, and studies using MK-801 (dizocilpine) have reported protection from ethanol-induced damage. The present study examined whether the administration of MK-801 during ethanol withdrawal would ameliorate ethanol-associated cell death in the interpositus nucleus of the cerebellum and behavioral deficits in a cerebellar dependent task. Long Evans rat pups were treated with ethanol (5.25 g/kg) in a binge-like manner on postnatal day 6 using intragastric intubation. Subjects then received an injection of MK-801 (0.5mg/kg) or vehicle during withdrawal, 30h after ethanol exposure. Rats were then trained on an eyeblink classical conditioning task as juveniles (40 days of age), and cerebellar interpositus nucleus numbers were assessed after conditioning. Ethanol-exposed subjects exhibited reductions in neuronal populations and behavioral deficits during eyeblink conditioning. However, MK-801 administration significantly attenuated observed deficiencies, suggesting a protective effect resulting from MK-801 treatment during ethanol withdrawal. These results support the role of NMDA receptor-mediated excitotoxicity as a component mechanism by which ethanol produces teratogenicity. Additionally, our findings support previous reports that have shown correlations between dependent measures of eyeblink classical-conditioning behavior and unbiased cell counts in the interpositus nucleus.
机译：在产后早期对啮齿动物受试者给药时，已证明暴饮暴食剂量的乙醇会严重破坏小脑和小脑依赖的工作。 N-甲基-d-天冬氨酸（NMDA）受体介导的与乙醇戒断有关的兴奋性毒性被认为是导致早期乙醇暴露引起的神经毒性作用的重要成分，并且使用MK-801（地佐西平）进行的研究报道了对乙醇的保护引起的损害。本研究检查了在戒断乙醇期间施用MK-801是否会改善小脑的中间核中与乙醇相关的细胞死亡以及小脑依赖性任务中的行为缺陷。在出生后第6天，使用胃内插管以暴饮暴食的方式用乙醇（5.25 g / kg）处理长Evans大鼠幼崽。然后受试者在戒酒期间，暴露于乙醇后30小时接受了MK-801（0.5mg / kg）或赋形剂注射。然后训练大鼠（约40天大）进行眨眼经典调理，并在调理后评估小脑中间核数。暴露于乙醇的受试者在眨眼条件下表现出神经元数量的减少和行为缺陷。然而，MK-801的给药显着减轻了观察到的缺陷，表明在撤回乙醇期间，MK-801处理可产生保护作用。这些结果支持NMDA受体介导的兴奋性毒性作为乙醇产生致畸性的成分机制的作用。此外，我们的发现支持了以前的报道，这些报道显示了眨眼经典条件行为的相关测量值与中间核中无偏细胞计数之间的相关性。

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