Raw test data-Synergistic Neurotoxicity Induced by Co-exposure to Heat Stress and Deoxynivalenol Contributes to Emotional Behavioral Deficits in Mice

This dataset contains the raw experimental data and analytical results generated from a study investigating the neurotoxic effects of combined heat stress and deoxynivalenol (DON) exposure on male ICR mice. Global climate change has intensified heat stress in animal production, which can cause emotional and cognitive dysfunction via activation of the hypothalamic-pituitary-adrenal (HPA) axis and hippocampal damage. Concurrently, hot and humid environments increase the risk of DON contamination in feed, and these two stressors often co-occur under practical farming conditions. However, their combined effects on the nervous system remain unclear. In this study, mice were subjected to single or combined exposure to heat stress (42 °C) and DON (2 mg/kg bw/day). Comprehensive datasets include behavioral test data (open field test and elevated zero maze), histopathological examination results (HE and Nissl staining), and molecular assay data (ELISA, qRT-PCR, and Western blotting) targeting key components of the HPA axis (CRH, ACTH, CORT), heat shock protein 70 (HSP70), neurotransmitters (5-HT, DA, E, NE), as well as key proteins in the ERK/CREB/BDNF signaling pathway and synaptic plasticity-related proteins (PSD95, SYN1). This data provides novel insights into the mechanisms by which heat stress and DON synergistically exacerbate emotional behavioral impairments through overactivating the HPA axis, disrupting neurotransmitter homeostasis, and inhibiting hippocampal neuroprotective pathways, serving as a valuable resource for understanding the neurotoxic effects of combined environmental stressors in animal production and public health.

本数据集包含一项关于联合热应激与脱氧雪腐镰刀菌烯醇（deoxynivalenol, DON）暴露对雄性ICR小鼠神经毒性影响的研究所产生的原始实验数据与分析结果。全球气候变化加剧了动物生产中的热应激问题，热应激可通过激活下丘脑-垂体-肾上腺（hypothalamic-pituitary-adrenal, HPA）轴以及造成海马体损伤，引发情绪与认知功能障碍。与此同时，高温高湿环境会提升饲料中DON污染的风险，且这两种应激因子在实际养殖环境中往往同时存在。然而，二者联合暴露对神经系统的影响尚不明确。本研究中，小鼠接受单独或联合暴露于热应激（42℃）与DON（2 mg/kg 体重/天）的处理。本数据集涵盖的综合数据包括：行为学测试数据（旷场实验与高架零迷宫实验结果）、组织病理学检查结果（苏木精-伊红（HE）染色与尼氏染色结果），以及针对HPA轴关键组分（促肾上腺皮质激素释放激素（CRH）、促肾上腺皮质激素（ACTH）、皮质酮（CORT））、热休克蛋白70（HSP70）、神经递质（5-羟色胺（5-HT）、多巴胺（DA）、肾上腺素（E）、去甲肾上腺素（NE））、丝裂原活化蛋白激酶/环腺苷酸应答元件结合蛋白/脑源性神经营养因子（ERK/CREB/BDNF）信号通路关键蛋白，以及突触可塑性相关蛋白（突触后致密蛋白95（PSD95）、突触蛋白1（SYN1））的分子检测数据（酶联免疫吸附测定（ELISA）、实时定量聚合酶链反应（qRT-PCR）与蛋白质印迹法（Western blotting））。本数据集为揭示热应激与DON通过过度激活HPA轴、破坏神经递质稳态以及抑制海马体神经保护通路，协同加重情绪行为损伤的机制提供了新视角，可为理解动物生产与公共卫生领域中复合环境应激因子的神经毒性效应提供宝贵的研究资源。