ArticleNeurobiology of disease2020
Activity-dependent dendritic elaboration requires Pten.
Article in Neurobiology of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed.
- Scaling of Neuronal Growth and Excitability Through Separable mTORC1 and mTORC2 Pathways.bioRxiv : the preprint server for biology · 2026Article
- PTEN Subcellular Localization Dictates Function.bioRxiv : the preprint server for biology · 2026Article
- Repurposing drugs for treating the neurobehavioral manifestations of PTEN hamartoma tumor syndrome.iScience · 2026Article
- Autism Spectrum Disorder: The Cerebellum, Genes, and Pathways.Neurology international · 2025Review
- PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors.Nature neuroscience · 2025Article
- mTORC2 Inhibition Improves Morphological Effects of PTEN Loss, But Does Not Correct Synaptic Dysfunction or Prevent Seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Disruption of mTORC1 rescues neuronal overgrowth and synapse function dysregulated by Pten loss.Cell reports · 2022Article
- Article
- PTEN Regulates Dendritic Arborization by Decreasing Microtubule Polymerization Rate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022Review
- Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity.Molecular autism · 2021Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Pten, a gene associated with autism spectrum disorder, is an upstream regulator of receptor tyrosine kinase intracellular signaling pathways that mediate extracellular cues to inform cellular development and activity-dependent plasticity. We therefore hypothesized that Pten loss would interfere with activity dependent dendritic growth. We investigated the effects of this interaction on the maturation of retrovirally labeled postnatally generated wild-type and Pten knockout granule neurons in male and female mouse dentate gyrus while using chemogenetics to manipulate the activity of the perforant path afferents. We find that enhancing network activity accelerates the dendritic outgrowth of wild-type, but not Pten knockout, neurons. This was specific to immature neurons during an early developmental window. We also examined synaptic connectivity and physiological measures of neuron maturation. The input resistance, membrane capacitance, dendritic spine morphology, and frequency of spontaneous synaptic events were not differentially altered by activity in wild-type versus Pten knockout neurons. Therefore, Pten and its downstream signaling pathways regulate the activity-dependent sculpting of the dendritic arbor during neuronal maturation.
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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.