ePoster

THE BENEFICIAL EFFECTS OF VOLUNTARY RUNNING ON ADULT NEUROGENESIS DEPEND ON THE AVAILABILITY OF BDNF IN THE BRAIN

Monique Klauschand 2 co-authors

Institute of Anatomy and Cell Biology, University Medicine Greifswald

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-203

Presentation

Date TBA

Board: PS01-07AM-203

Poster preview

THE BENEFICIAL EFFECTS OF VOLUNTARY RUNNING ON ADULT NEUROGENESIS DEPEND ON THE AVAILABILITY OF BDNF IN THE BRAIN poster preview

Event Information

Poster Board

PS01-07AM-203

Abstract

The subgranular zone of the dentate gyrus (DG) is an important site where the adult hippocampus neurogenesis occurs. In addition to its essential role in development, brain-derived neurotrophic factor (BDNF) also acts in the postnatal brain, particularly in processes related to neural plasticity, learning, and memory. It is known that reduced BDNF levels impair memory. Voluntary running has been shown to improve cognitive abilities, protect against cognitive decline, and increase BDNF levels in the hippocampus. Here, we investigate the role of BDNF and voluntary running on adult hippocampal neurogenesis in adult mice using adult male heterozygous BDNF-deficient mice and their age-matched control siblings. The behavior of these mice was analyzed, as was the rate of adult neurogenesis, which was monitored using the marker doublecortin (DCX), either under normal conditions (“non-runners”) or with unlimited access to a running wheel (“runners”) for three weeks. Heterozygous BDNF-deficient mice differ from +/+ mice in their running wheel behavior, especially during the dark phase. During this phase, +/- mice also differ in their feeding behavior and body weight change. Comparable numbers of DCX-positive cells can be observed in adult +/+ mice and +/- “non-runner” mice. Running induces a strong increase in the number of DCX-cells in +/+ mice, and a weaker increase in +/- mice. These results indicate that reduced levels of BDNF in the brain did not affect basal adult neurogenesis, but that plasticity-induced changes in adult neurogenesis seem to depend on the availability of normal levels of BDNF.

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