ePoster

LOW-GRADE CHRONIC HIPPOCAMPAL INFLAMMATION PROMOTES MICROGLIAL REACTIVITY AND BLUNTS EXERCISE-INDUCED NEUROGENESIS IN RATS

Sarah Nicolasand 4 co-authors

Centre de Recherches sur la Cognition Animale (CRCA), Centre de Biologie Intégrative (CBi), Université de Toulouse, CNRS

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-196

Presentation

Date TBA

Board: PS01-07AM-196

Poster preview

LOW-GRADE CHRONIC HIPPOCAMPAL INFLAMMATION PROMOTES MICROGLIAL REACTIVITY AND BLUNTS EXERCISE-INDUCED NEUROGENESIS IN RATS poster preview

Event Information

Poster Board

PS01-07AM-196

Abstract

Adult hippocampal neurogenesis (AHN), the ability of the hippocampus to generate new neurons across the lifespan, maintains memory and the regulation of emotion. The pro-inflammatory cytokine interleukin-1β (IL-1β) is elevated in the hippocampus with age and Alzheimer’s disease and reduces AHN and impairs memory. Conversely, exercise enhances AHN and associated behaviours in healthy rodents, however its effects in an inflamed hippocampus remain unclear. Here, we investigated the impact of chronic hippocampal IL-1β overexpression and exercise on memory, AHN and microglia reactivity in adult male rats. After lentiviral delivery of IL-1β or scrambled control in the hippocampus, animals were housed with or without running wheels for 8 weeks. IL-1β impaired pattern separation in both sedentary and exercising animals. Exercise increased the number of doublecortin+ cells (AHN) in the hippocampus, an effect blunted by IL-1β. Microglial analyses revealed that exercise reduces IL-1β-associated increases in Iba+ cells and soma size, and modulated lipid droplet accumulation in the hippocampus. Transcriptomic analysis of isolated hippocampal microglia showed that exercise downregulated chemotactic and pro-inflammatory gene expression programs in control rats but upregulated immune pathways, including leukocyte migration and cytokine signalling in IL-1β-treated rats. While exercise promotes AHN and suppresses microglial inflammation under physiological conditions, prior IL-1β-induced neuroinflammation negates its proneurogenic and anti-inflammatory effects. Our findings highlight inflammatory context as a critical determinant of exercise efficacy relevant to ageing and neurodegeneration.

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