预暴露于乙醇后果蝇Stat92E信号传导

IF 2.9 Q2 NEUROSCIENCES Neuroscience Insights Pub Date : 2023-01-01 DOI:10.1177/26331055221146755
Alexandria Wilson, Erica M Periandri, Mackenzie Sievers, Emily Petruccelli
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引用次数: 0

摘要

反复接触酒精会改变神经分子信号,影响酒精使用障碍(AUD)潜在的急性和长期行为。最近的动物模型研究表明,保守的JAK/STAT通路发生了变化,这是一种与发育和先天免疫系统相关的信号通路。乙醇暴露如何影响神经细胞内STAT信号目前尚不清楚。在这里,我们研究了果蝇Stat92E在乙醇诱导的运动、信号活性和下游转录反应中的作用。研究结果表明,在先前暴露于乙醇的果蝇中,表达Stat92E-RNAi会导致乙醇诱导的过度活跃增强。此外,在重复乙醇暴露后,检测到Stat92E本身的选择性剪接,尽管下游转录活性没有变化。这项工作增加了我们对乙醇暴露后改变的神经分子信号的理解,并表明STAT信号可能是AUD治疗的相关靶点。
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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Drosophila Stat92E Signaling Following Pre-exposure to Ethanol.

Repeated exposure to alcohol alters neuromolecular signaling that influences acute and long-lasting behaviors underlying Alcohol Use Disorder (AUD). Recent animal model research has implicated changes in the conserved JAK/STAT pathway, a signaling pathway classically associated with development and the innate immune system. How ethanol exposure impacts STAT signaling within neural cells is currently unclear. Here, we investigated the role of Drosophila Stat92E in ethanol-induced locomotion, signaling activity, and downstream transcriptional responses. Findings suggest that expressing Stat92E-RNAi causes enhanced ethanol-induced hyperactivity in flies previously exposed to ethanol. Furthermore, alternative splicing of Stat92E itself was detected after repeated ethanol exposure, although no changes were found in downstream transcriptional activity. This work adds to our growing understanding of altered neuromolecular signaling following ethanol exposure and suggests that STAT signaling may be a relevant target to consider for AUD treatment.

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来源期刊
Neuroscience Insights
Neuroscience Insights Neuroscience-Neuroscience (all)
CiteScore
6.10
自引率
0.00%
发文量
24
审稿时长
9 weeks
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