Abstract
The continuous generation of new neurons in the adult mammalian hippocampus is a form of neural plasticity that modulates learning and memory functions, and also emotion (anxiety and depression). Among the factors known to modulate adult hippocampal neurogenesis and brain function, lipocalin-2 (LCN2) was recently described as a key regulator of neural stem cells (NSCs) proliferation and commitment, with impact on several dimensions of behaviour. Herein, we evaluated whether voluntary running, a well-known regulator of cell genesis, rescue the deficient adult hippocampal neurogenesis observed in mice lacking LCN2. We observed that running, by counteracting oxidative stress in NSCs, reverses LCN2-null mice defective hippocampal neurogenesis, as it promotes NSCs cell cycle progression and maturation, resulting in a partial reduction in anxiety and improved contextual behaviour. Together, these findings demonstrate that running is a positive modulator of adult hippocampal neurogenesis and behaviour in mice lacking LCN2, by impacting on the antioxidant kinetics of NSCs.
Highlights
In the adult mammalian brain, the continuous generation of new neurons in the subgranular zone (SGZ) of the dentate gyrus (DG) in the hippocampus contributes to modulate local neural plasticity and network dynamics[1]
We investigated whether voluntary running could revert the impairments in the process of hippocampal neurogenesis observed in the absence of LCN2
LCN2-null mice hippocampal quiescent neural stem cells (NSCs) respond to voluntary running, promoting progenitors proliferation
Summary
In the adult mammalian brain, the continuous generation of new neurons in the subgranular zone (SGZ) of the dentate gyrus (DG) in the hippocampus contributes to modulate local neural plasticity and network dynamics[1]. Analysis of the total number of BrdU+ cells, as a measure of cell survival in the SGZ, revealed that exercise significantly increased this population (running effect: F1,14 = 19.9, p = 0.0005), both in Wt (p = 0.007) and LCN2-null SGZ (p = 0.03), compared to the respective sedentary genotypes (Fig. 1c,d).
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