ArticleFrontiers in neuroscience2016
GluN2B-Containg NMDA Receptors on Adult-Born Granule Cells Contribute to the Antidepressant Action of Fluoxetine.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Effect of adult hippocampal neurogenesis on pattern separation and its applications.Cognitive neurodynamics · 2024Article
- Exosomes induce neurogenesis of pluripotent P19 cells.Stem cell reviews and reports · 2023Article
- Stress-Related Dysfunction of Adult Hippocampal Neurogenesis-An Attempt for Understanding Resilience?International journal of molecular sciences · 2021Review
- Modulation of Aversive Memory by Adult Hippocampal Neurogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- Adult hippocampal neurogenesis and cognitive flexibility - linking memory and mood.Nature reviews. Neuroscience · 2017Review
- Cognitive Decline in Neuronal Aging and Alzheimer's Disease: Role of NMDA Receptors and Associated Proteins.Frontiers in neuroscience · 2017Review
- Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Ablation of adult neurogenesis in mice has revealed that young adult-born granule cells (abGCs) are required for some of the behavioral responses to antidepressants (ADs), yet the mechanism by which abGCs contribute to AD action remains unknown. During their maturation process, these immature neurons exhibit unique properties that could underlie their ability to influence behavioral output. In particular, abGCs in the DG exhibit a period of heightened plasticity 4-6 weeks after birth that is mediated by GluN2B-expressing NMDA receptors. The functional contribution of this critical window to AD responsiveness is unclear. Here, we determined the behavioral and neurogenic responses to the AD fluoxetine (FLX) in mice lacking GluN2B-containing NMDA receptors in abGCs. We found that these mice exhibited an attenuated response to FLX in a neurogenesis-dependent behavioral assay of FLX action, while neurogenesis-independent behaviors were unaffected by GluN2B deletion. In addition, deletion of GluN2B attenuated FLX-induced increases in dendritic complexity of abGCs suggesting that the blunted behavioral efficacy of FLX may be caused by impaired differentiation of young abGCs.
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Registered trials
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