Dataset for "Hippocampal BDNF mediated anxiety-like behaviours induced by obesogenic diet withdrawal."

This data was used in the production of the article entitled "Hippocampal BDNF mediated anxiety-like behaviours induced by obesogenic diet withdrawal." published in 2022 at Behavioural Brain Research (ISSN: 0166-4328) (DOI: 10.1016/j.bbr.2022.114077). Abstract (DOI: 10.1016/j.bbr.2022.114077) Obesogenic diets (ODs) consumption is associated with anxiety-like behaviour and negative changes in hippocampal BDNF. At the same time, interrupting OD intake, OD withdrawal (WTD), can bring health benefits, but previous studies reported the development of anxiety-like behaviours. The present work aimed to assess the relationship between anxiety-like behaviour with hippocampal BDNF in a WTD rodent model. Male Wistar rats (60d old) were fed a high-sugar/high-fat (HSHF) diet for 30d (n=32), and half of them were transitioned to a control diet for 48 h (n=16) afterwards. The control group (n=16) was fed a control diet across the whole experiment. Besides increasing anxiety-like behaviours and lowering sociability, the WTD led to an increase in BDNF in the dentate gyrus and the CA1 of the hippocampus. It also decreased locomotor activity in both OF and EPM, however, they did not significantly interfere with the other behavioural parameters analysed. Western blotting analysis revealed that the increase in BDNF likely occurred in the mature forms (14kD monomer and 28kD dimer). The mediation models analyses suggested that the effect of WTD on anxiety-like behaviour was driven by hippocampal BDNF, this mediation of effect was region-dependent. Our results also suggested that mature BDNF forms (14kD and 28kD) were responsible. The present work brought light to a possible new role for mature BDNF, although it is generally associated with beneficial features, it can also be part of the genesis of anxiety-like behaviours and sociability aspects on WTD models. It contains the .csv file with the data used in the publication. Researcher in charge: Debora Estadella Researcher in charge of data collection: Breno Picin Casagrande Date of data collection: 01/04/2018 - 1/12/2019 Financial support: CAPES - Brazil, FAPESP (2017/25420-3), CNPq

本数据集用于2022年发表于《行为脑研究》（Behavioural Brain Research，ISSN: 0166-4328，DOI: 10.1016/j.bbr.2022.114077）、题为《肥胖饮食戒断诱导的焦虑样行为由海马脑源性神经营养因子（Brain-Derived Neurotrophic Factor, BDNF）介导》的论文制作。

摘要：致肥胖饮食（Obesogenic Diet, OD）的摄入与焦虑样行为及海马BDNF的负面变化相关。与此同时，中断致肥胖饮食摄入即致肥胖饮食戒断（WTD），虽可带来健康益处，但既往研究显示其会引发焦虑样行为。本研究旨在评估致肥胖饮食戒断啮齿动物模型中，焦虑样行为与海马BDNF的关联。

将60日龄的雄性Wistar大鼠32只给予高糖高脂（High-Sugar/High-Fat, HSHF）饮食30天，其中16只随后转换为对照饮食并持续48小时（n=16）；剩余16只全程给予对照饮食（n=16）。

研究结果显示，致肥胖饮食戒断除增加焦虑样行为、降低社交能力外，还可使海马齿状回与CA1区的BDNF水平升高；同时会降低大鼠在旷场实验（Open Field, OF）与高架十字迷宫实验（Elevated Plus Maze, EPM）中的自主活动水平，但对其他分析的行为学参数无显著影响。蛋白质印迹（Western Blotting）分析显示，BDNF水平的升高主要发生于其成熟形式：14kD单体与28kD二聚体。中介效应模型分析表明，致肥胖饮食戒断对焦虑样行为的影响由海马BDNF介导，且该介导效应具有脑区依赖性。本研究结果还证实，成熟BDNF形式（14kD与28kD）是该效应的核心介导因子。

本研究揭示了成熟BDNF的一种潜在新功能——尽管其通常与多种有益生物学特性相关，但在致肥胖饮食戒断模型中，它也可能参与焦虑样行为与社交能力异常的发生过程。

本数据集包含该论文所用的.csv格式数据。
课题负责人：Debora Estadella
数据采集负责人：Breno Picin Casagrande
数据采集周期：2018年4月1日 — 2019年12月1日
资助单位：巴西高等教育人员发展协调局（CAPES）、圣保罗研究基金会（FAPESP，编号2017/25420-3）、巴西国家科学技术发展委员会（CNPq）