ArticleCellular and molecular life sciences : CMLS2016
Retroviral induction of GSK-3β expression blocks the stimulatory action of physical exercise on the maturation of newborn neurons.
Article in Cellular and molecular life sciences : CMLS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- How to Prevent and/or Revert Alzheimer's Disease Continuum During Preclinical Phases.Journal of Alzheimer's disease reports · 2023Review
- Steps towards standardized quantification of adult neurogenesis.Nature communications · 2020Review
- Intracellular A53T Mutant α-Synuclein Impairs Adult Hippocampal Newborn Neuron Integration.Frontiers in cell and developmental biology · 2020Article
- Facilitating Granule Cell Survival and Maturation in Dentate Gyrus With Baicalin for Antidepressant Therapeutics.Frontiers in pharmacology · 2020Article
- Tau Phosphorylation and Aggregation in the Developing Human Brain.Journal of neuropathology and experimental neurology · 2019Article
- Exercising New Neurons to Vanquish Alzheimer Disease.Brain plasticity (Amsterdam, Netherlands) · 2018Review
- Identifying molecular mediators of environmentally enhanced neurogenesis.Cell and tissue research · 2018Review
- Prenatal Alcohol Exposure Leads to Enhanced Serine 9 Phosphorylation of Glycogen Synthase Kinase-3β (GSK-3β) in the Hippocampal Dentate Gyrus of Adult Mouse.Alcoholism, clinical and experimental research · 2017Article
- Article
- GSK-3β Overexpression Alters the Dendritic Spines of Developmentally Generated Granule Neurons in the Mouse Hippocampal Dentate Gyrus.Frontiers in neuroanatomy · 2017Article
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adult hippocampal neurogenesis (AHN) is a key process for certain types of hippocampal-dependent learning. Alzheimer's disease (AD) is accompanied by memory deficits related to alterations in AHN. Given that the increased activity of GSK-3β has been related to alterations in the population of hippocampal granule neurons in AD patients, we designed a novel methodology by which to induce selective GSK-3β overexpression exclusively in newborn granule neurons. To this end, we injected an rtTA-IRES-EGFP-expressing retrovirus into the hippocampus of tTO-GSK-3β mice. Using this novel retroviral strategy, we found that GSK-3β caused a cell-autonomous impairment of the morphological and synaptic maturation of newborn neurons. In addition, we examined whether GSK-3β overexpression in newborn neurons limits the effects of physical activity. While physical exercise increased the number of dendritic spines, the percentage of mushroom spines, and the head diameter of the same in tet-OFF cells, these effects were not triggered in tet-ON cells. This observation suggests that GSK-3β blocks the stimulatory actions of exercise. Given that the activity of GSK-3β is increased in the brains of individuals with AD, these data may be relevant for non-pharmacological therapies for AD.
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