ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Age-independent synaptogenesis by phosphoinositide 3 kinase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 110 citations in OpenAlex.
- Activity drives local CaMKII synthesis and subcellular localization via autophosphorylation-dependent pathways.bioRxiv : the preprint server for biology · 2025Article
- tRNA modification enzyme-dependent redox homeostasis regulates synapse formation and memory.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Biological aging of two innate behaviors of Drosophila melanogaster: Escape climbing versus courtship learning and memory.PloS one · 2024Article
- tRNA modification enzyme-dependent redox homeostasis regulates synapse formation and memory.bioRxiv : the preprint server for biology · 2023Article
- A whole transcriptome profiling analysis for antidepressant mechanism of Xiaoyaosan mediated synapse loss via BDNF/trkB/PI3K signal axis in CUMS rats.BMC complementary medicine and therapies · 2023Article
- Evolution of central neural circuits: state of the art and perspectives.Nature reviews. Neuroscience · 2022Review
- Functional specialization of different PI3K isoforms for the control of neuronal architecture, synaptic plasticity, and cognition.Science advances · 2022Article
- Alignment between glioblastoma internal clock and environmental cues ameliorates survival in Drosophila.Communications biology · 2022Article
- Activity-regulated growth of motoneurons at the neuromuscular junction is mediated by NADPH oxidases.Frontiers in cellular neuroscience · 2022Article
- Reduced Insulin Signaling Targeted to Serotonergic Neurons but Not Other Neuronal Subtypes Extends Lifespan inFrontiers in aging neuroscience · 2022Article
- Downregulation of PIK3CB Involved in Alzheimer's Disease via Apoptosis, Axon Guidance, and FoxO Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Insulin signaling mediates neurodegeneration in glioma.Life science alliance · 2021Article
- Vegetarian diets, circulating miRNA expression and healthspan in subjects living in the Blue Zone.Precision clinical medicine · 2020Article
- Phosphoinositide-3-kinase regulatory subunit 1 gene polymorphisms are associated with schizophrenia and bipolar disorder in the Han Chinese population.Metabolic brain disease · 2020Article
- PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.Molecular biology of the cell · 2020Article
- CCB is Involved in Actin-Based Axonal Transport of Selected Synaptic Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- PI3Kinase-p110δ Overexpression Impairs Dendritic Morphogenesis and Increases Dendritic Spine Density.Frontiers in molecular neuroscience · 2020Article
- The TOR Pathway at the Neuromuscular Junction: More Than a Metabolic Player?Frontiers in molecular neuroscience · 2020Review
- Lineage-specific determination of ring neuron circuitry in the central complex ofBiology open · 2019Article
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3 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapses are specialized communication points between neurons, and their number is a major determinant of cognitive abilities. These dynamic structures undergo developmental- and activity-dependent changes. During brain aging and certain diseases, synapses are gradually lost, causing mental decline. It is, thus, critical to identify the molecular mechanisms controlling synapse number. We show here that the levels of phosphoinositide 3 kinase (PI3K) regulate synapse number in both Drosophila larval motor neurons and adult brain projection neurons. The supernumerary synapses induced by PI3K overexpression are functional and elicit changes in behavior. Remarkably, PI3K activation induces synaptogenesis in aged adult neurons as well. We demonstrate that persistent PI3K activity is necessary for synapse maintenance. We also report that PI3K controls the expression and localization of synaptic markers in human neuroblastoma cells, suggesting that PI3K synaptogenic activity is conserved in humans. Thus, we propose that PI3K stimulation can be applied to prevent or delay synapse loss in normal aging and in neurological disorders.
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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.