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

Description

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.

Steps to reproduce

All data in this study were generated from standardized in vivo experiments on 7-week-old ICR mice: first, a heat stress model with temperature gradients was established to screen 42 °C as the optimal stress temperature and male mice as experimental subjects; then the male mice were randomly divided into four groups (control, heat stress, DON (2 mg/kg bw/day) exposure, and combined heat stress + DON exposure) and treated for 2 weeks. Behavioral assessments (open field test and elevated zero maze test) were conducted using the Smart V3.0 tracking system and SSC-D213 behavioral recording system. After the tests, mouse blood and hippocampal tissues were collected for subsequent assays: hematoxylin-eosin (HE) and Nissl staining were used for histopathological observation of hippocampal neurons; serum levels of HPA axis-related hormones, HSP70 and neurotransmitters were detected via commercial ELISA kits with an ELISA reader at 450 nm; total RNA was extracted from hippocampal tissues by the Trizol method, and qRT-PCR was performed with PrimeScript™ RT Master Mix kit and specific synthesized primers to quantify gene expression; total protein was extracted using RIPA lysis buffer (supplemented with phosphatase and protease inhibitors), protein concentration was determined by BCA assay, and Western blotting was conducted via 10% SDS-PAGE, membrane transfer, and incubation with specific primary and secondary antibodies (with defined dilution ratios). All experimental data were processed by Smart V3.0 tracking software and statistically analyzed by one-way ANOVA using GraphPad Prism 8, with results presented as mean ± SEM.

Institutions

• Shanxi Agricultural University

  Shanxi, Xiaodian

Categories

Funders

• the Science and Technology Innovation Teams of Shanxi Province

  Grant ID: 202304051001041

Licence