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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Cholinergic system and exploratory behavior are changed after weekly-binge ethanol exposure in zebrafish
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Cholinergic system and exploratory behavior are changed after weekly-binge ethanol exposure in zebrafish

机译：在斑马鱼的每周狂欢乙醇暴露后，胆碱能系统和探索性行为发生变化

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摘要

Binge drinking is characterized by excessive alcohol consumption in a short period of time and is associated with a poor quality of life. Zebrafish are commonly used to investigate neurochemical, behavioral, and genetic parameters associated with ethanol (EtOH) exposure. However, few studies have used zebrafish as a model to investigate binge EtOH exposure. In order to elucidate the potential neurobehavioral impairments evoked by binge EtOH exposure in zebrafish, animals were immersed in 1.4% EtOH for 30 min three consecutive times with intervals of one week. Neurobehavioral parameters were analyzed immediately following the third exposure, as well as 2 and 9 days later. Brain choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were reduced 9 days after the treatment. Thiobarbituric acid-reactive species and dichlorodihydrofluorescein levels were increased immediately after the treatment, but both returned to normal levels 2 days after the treatment. Catalase and glutathione reductase were impaired 2 and 9 days after the treatment. No alteration was observed in superoxide dismutase and glutathione peroxidase activities. EtOH treatment did not alter brain expression of inflammatory genes such as il-1 beta, il-10, and tnf-alpha. Zebrafish displayed anxiolytic-like behavior immediately after the last exposure, though there was no behavioral alteration observed 9 days after the treatment. Therefore, binge EtOH exposure in zebrafish leads to long lasting brain cholinergic alteration, probably related to oxidative stress immediately after the exposure, which is independent of classical inflammatory markers.
机译：狂欢饮酒的特点是在短时间内过量的酒精消耗，与差的生活质量有关。斑马鱼通常用于研究与乙醇（EtOH）暴露相关的神经化学，行为和遗传参数。然而，很少有研究用Zebrafish作为调查狂犬病暴露的模型。为了阐明在斑马鱼中的斑点EtOH暴露中引起的潜在神经障碍障碍，将动物浸入1.4％EtOH中，连续三次以一周的间隔浸出30分钟。在第三次曝光后立即分析神经兽性参数，以及2和9天后分析。治疗后9天减少了脑胆碱乙酰转移酶（聊天）和乙酰胆碱酯酶（ACHE）活性。治疗后立即增加硫氨基吡咯酸反应性物种和二氯二氢荧光素水平，但两者在治疗后2天恢复到正常水平。过氧化氢酶和谷胱甘肽还原酶在治疗后2和9天受损。在超氧化物歧化酶和谷胱甘肽过氧化物酶活性中没有观察到不改变。 EtOH治疗没有改变炎症基因的脑表达，例如IL-1β，IL-10和TNF-α。斑马鱼在最后一次暴露后立即显示出抗焦虑的行为，尽管治疗后9天没有观察到行为改变。因此，斑马鱼中的泪液EtOH暴露导致持久的脑胆碱能改变，可能与曝光后立即氧化应激，这与典型炎症标志物无关。

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