ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
The p75NTR Influences Cerebellar Circuit Development and Adult Behavior via Regulation of Cell Cycle Duration of Granule Cell Progenitors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Redundancy of p75NTR neurotrophin receptor function in development, growth and fertility in the rat.Transgenic research · 2024Article
- Neuropeptides and Their Roles in the Cerebellum.International journal of molecular sciences · 2024Review
- Building better brains: the pleiotropic function of neurotrophic factors in postnatal cerebellar development.Frontiers in molecular neuroscience · 2023Review
- Excess cerebellar granule neurons induced by the absence of p75NTR during development elicit social behavior deficits in mice.Frontiers in molecular neuroscience · 2023Article
- Immune activation of the p75 neurotrophin receptor: implications in neuroinflammation.Frontiers in molecular neuroscience · 2023Article
- Article
- Reduced Granule Cell Proliferation and Molecular Dysregulation in the Cerebellum of Lysosomal Acid Phosphatase 2 (ACP2) Mutant Mice.International journal of molecular sciences · 2021Article
- Up-regulation of the p75 neurotrophin receptor is an essential mechanism for HIV-gp120 mediated synaptic loss in the striatum.Brain, behavior, and immunity · 2020Article
- Signaling via the p75 neurotrophin receptor facilitates amyloid-β-induced dendritic spine pathology.Scientific reports · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Development of brain circuitry requires precise regulation and timing of proliferation and differentiation of neural progenitor cells. The p75 neurotrophin receptor (p75NTR) is highly expressed in the proliferating granule cell precursors (GCPs) during development of the cerebellum. In a previous paper, we showed that proNT3 promoted GCP cell cycle exit via p75NTR. Here we used genetically modified rats and mice of both sexes to show that p75NTR regulates the duration of the GCP cell cycle, requiring activation of RhoA. Rats and mice lacking p75NTR have dysregulated GCP proliferation, with deleterious effects on cerebellar circuit development and behavioral consequences persisting into adulthood. In the absence of p75NTR, the GCP cell cycle is accelerated, leading to delayed cell cycle exit, prolonged GCP proliferation, increased glutamatergic input to Purkinje cells, and a deficit in delay eyeblink conditioning, a cerebellum-dependent form of learning. These results demonstrate the necessity of appropriate developmental timing of the cell cycle for establishment of proper connectivity and associated behavior.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.