Binge-like Alcohol Administration Alters Decision Making in an Adolescent Rat Model: Role of N-Methyl-D-Aspartate Receptor Signaling

Stresses Pub Date : 2023-12-22 DOI:10.3390/stresses4010001
Camila Arce, Rodrigo G. Mira, Matías Lira, W. Cerpa
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Abstract

Alcohol is one of the most used legal drugs abused worldwide, and its consumption is associated with high mortality and morbidity rates. There is an increasing concern about the starting age of consumption of this drug since it has become evident that it is at younger ages. The so-called “pattern of consumption by binge” corresponds to ingesting large amounts of alcohol in a short period and is the most popular among young people. Previous studies show that alcohol causes damage in different areas, such as the hippocampus, hypothalamus, and prefrontal cortex, and adolescents are more susceptible to alcohol toxicity. Alcohol inhibits the membrane glutamate receptor, NMDA-type glutamate receptors (NMDAR). Using a binge-like alcohol administration protocol in adolescent rats (PND25), we investigate decision making through the attentional set-shifting test (ASST) and alterations in the NMDAR signaling in related areas. We observe an impairment in executive function without alterations in NMDAR abundance. However, binge alcohol changes NMDAR signaling and decreases quantity in the synapse, mainly in the hippocampus and hypothalamus. We suggest that prefrontal cortex impairment could arise from damaged connections with the hippocampus and hypothalamus, affecting the survival pathway and memory and learning process.
狂饮型酒精管理会改变青少年大鼠模型的决策:N-Methyl-D-Aspartate 受体信号的作用
酒精是全世界滥用最多的合法药物之一,其消费与高死亡率和发病率有关。人们越来越关注这种药物的消费起始年龄,因为很明显,这种药物的消费起始年龄越来越小。所谓的 "狂欢消费模式 "是指在短时间内摄入大量酒精,在年轻人中最为流行。以往的研究表明,酒精会对海马、下丘脑和前额叶皮层等不同区域造成损害,而青少年更容易受到酒精中毒的影响。酒精会抑制膜谷氨酸受体--NMDA 型谷氨酸受体(NMDAR)。我们在青少年大鼠(PND25)中使用了一种类似酗酒的给药方案,通过注意力集合转移测试(ASST)和相关区域中 NMDAR 信号的改变来研究决策制定。我们观察到执行功能受损,但 NMDAR 丰度没有发生变化。然而,酗酒会改变 NMDAR 信号传递并减少突触中的数量,主要是在海马和下丘脑。我们认为,前额叶皮质受损可能源于与海马和下丘脑的连接受损,从而影响生存途径以及记忆和学习过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
4.70
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