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<p>Exercise training promotes brain health, yet the underlying mechanisms remain unclear. ∆FOSB, a transcription factor involved in neuroplasticity, stress-, cognition- and reward-related behavior, accumulates in response to repetitive neuronal stimulation due to its unusual protein stability and can thus serve as a proxy for chronic neuronal activation. This study employed voluntary wheel running (VWR), an animal model for exercise training, in male and female Wistar rats to quantify VWR-induction of ∆FOSB in 44 brain regions implicated in stress, cognition and reward. Using network analysis, we examined broader patterns of co-activation and changes in network topology (<i>e</i>.<i>g</i>. centrality, small-world-likeness) of this comprehensive map of brain regions. Four weeks of VWR improved metabolic health, independent of sex, and females ran more than males. Notably, semi-automated quantification of ∆FOSB-immunoreactivity revealed VWR regulation of ∆FOSB in several cortical, striatal, hippocampal, hypothalamic and midbrain regions, which was more pronounced in females. VWR altered several parameters of ∆FOSB co-activation networks, decreasing network density while increasing global efficiency in both sexes, and was associated with greater cortical centrality. These findings demonstrate that VWR-mediated chronic neuronal activation extends beyond previously studied brain regions and that habitual VWR shifts hierarchy to more cortical regions. Because ∆FOSB overexpression is associated with lower neuronal excitability, the current ∆FOSB brain atlas and network co-activation dataset extends our understanding of the impact of VWR on brain neuroplasticity and provides a framework for future mechanistic studies into ∆FOSB-mediated changes in neuronal excitability during habitual VWR and subsequent effects on stress-, cognition- and reward-related behavior.</p>

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Brain-wide induction of ΔFOSB and altered co-activation networks in a rat model for exercise training

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月26日

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  • Marene H. Hardonk,
  • Anna H. Vuuregge,
  • Tom P. Hellings,
  • Leslie Eggels,
  • Wayne I.G.R. Ritsema,
  • Khalid Lamuadni,
  • Unga A. Unmehopa,
  • Gideon F. Meerhoff,
  • Andries Kalsbeek,
  • Paul J. Lucassen,
  • Anouk Schrantee,
  • Susanne E. la Fleur,
  • Joram D. Mul

摘要

Exercise training promotes brain health, yet the underlying mechanisms remain unclear. ∆FOSB, a transcription factor involved in neuroplasticity, stress-, cognition- and reward-related behavior, accumulates in response to repetitive neuronal stimulation due to its unusual protein stability and can thus serve as a proxy for chronic neuronal activation. This study employed voluntary wheel running (VWR), an animal model for exercise training, in male and female Wistar rats to quantify VWR-induction of ∆FOSB in 44 brain regions implicated in stress, cognition and reward. Using network analysis, we examined broader patterns of co-activation and changes in network topology (e.g. centrality, small-world-likeness) of this comprehensive map of brain regions. Four weeks of VWR improved metabolic health, independent of sex, and females ran more than males. Notably, semi-automated quantification of ∆FOSB-immunoreactivity revealed VWR regulation of ∆FOSB in several cortical, striatal, hippocampal, hypothalamic and midbrain regions, which was more pronounced in females. VWR altered several parameters of ∆FOSB co-activation networks, decreasing network density while increasing global efficiency in both sexes, and was associated with greater cortical centrality. These findings demonstrate that VWR-mediated chronic neuronal activation extends beyond previously studied brain regions and that habitual VWR shifts hierarchy to more cortical regions. Because ∆FOSB overexpression is associated with lower neuronal excitability, the current ∆FOSB brain atlas and network co-activation dataset extends our understanding of the impact of VWR on brain neuroplasticity and provides a framework for future mechanistic studies into ∆FOSB-mediated changes in neuronal excitability during habitual VWR and subsequent effects on stress-, cognition- and reward-related behavior.