ArticleProceedings of the National Academy of Sciences of the United States of America2008
Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 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
128 citing papers in PubMed, 214 citations in OpenAlex.
- Trial
- Drp1-Mediated Mitochondrial Fission Is Essential for Chemical-Induced Neuronal Transdifferentiation from Human Primary Fibroblasts.Journal of molecular neuroscience : MN · 2025Article
- Bcl-2 and Bcl-xL in Diabetes: Contributions to Endocrine Pancreas Viability and Function.Biomedicines · 2025Review
- CoCrMo nanoparticle induces neurotoxicity mediated via mitochondrial dysfunction: a study model for implant derived nanoparticle effects.Nanotoxicology · 2024Article
- Mechanisms of Modulation of Mitochondrial Architecture.Biomolecules · 2023Review
- Mitochondrial Bcl-xL promotes brain synaptogenesis by controlling non-lethal caspase activation.iScience · 2023Article
- BAX regulates dendritic spine development via mitochondrial fusion.Neuroscience research · 2022Article
- Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL.Nutrition research (New York, N.Y.) · 2022Article
- Revealing the Impact of Mitochondrial Fitness During Early Neural Development Using Human Brain Organoids.Frontiers in molecular neuroscience · 2022Review
- Energy matters: presynaptic metabolism and the maintenance of synaptic transmission.Nature reviews. Neuroscience · 2022Review
- Neuroglial Senescence, α-Synucleinopathy, and the Therapeutic Potential of Senolytics in Parkinson's Disease.Frontiers in neuroscience · 2022Review
- Bcl-xL Is Required by Primary Hippocampal Neurons during Development to Support Local Energy Metabolism at Neurites.Biology · 2021Article
- Involvement of Bcl-xL in Neuronal Function and Development.International journal of molecular sciences · 2021Review
- SENP3 Promotes an Mff-Primed Bcl-xFrontiers in cell and developmental biology · 2021Article
- Oxidative stress battles neuronal Bcl-xL in a fight to the death.Neural regeneration research · 2021Article
- Cell Death Related Proteins Beyond Apoptosis in the CNS.Frontiers in cell and developmental biology · 2021Review
- Caspases in the Developing Central Nervous System: Apoptosis and Beyond.Frontiers in cell and developmental biology · 2021Review
- Glutamatergic Dysfunction and Synaptic Ultrastructural Alterations in Schizophrenia and Autism Spectrum Disorder: Evidence from Human and Rodent Studies.International journal of molecular sciences · 2020Review
- Regulation of Cell Death by Mitochondrial Transport Systems of Calcium and Bcl-2 Proteins.Membranes · 2020Review
- Development of Conformational Antibodies to Detect Bcl-xL's Amyloid Aggregates in Metal-Induced Apoptotic Neuroblastoma Cells.International journal of molecular sciences · 2020Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 3 countries.
Funding
Abstract
Maturation of neuronal synapses is thought to involve mitochondria. Bcl-xL protein inhibits mitochondria-mediated apoptosis but may have other functions in healthy adult neurons in which Bcl-xL is abundant. Here, we report that overexpression of Bcl-xL postsynaptically increases frequency and amplitude of spontaneous miniature synaptic currents in rat hippocampal neurons in culture. Bcl-xL, overexpressed either pre or postsynaptically, increases synapse number, the number and size of synaptic vesicle clusters, and mitochondrial localization to vesicle clusters and synapses, likely accounting for the changes in miniature synaptic currents. Conversely, knockdown of Bcl-xL or inhibiting it with ABT-737 decreases these morphological parameters. The mitochondrial fission protein, dynamin-related protein 1 (Drp1), is a GTPase known to localize to synapses and affect synaptic function and structure. The effects of Bcl-xL appear mediated through Drp1 because overexpression of Drp1 increases synaptic markers, and overexpression of the dominant-negative dnDrp1-K38A decreases them. Furthermore, Bcl-xL coimmunoprecipitates with Drp1 in tissue lysates, and in a recombinant system, Bcl-xL protein stimulates GTPase activity of Drp1. These findings suggest that Bcl-xL positively regulates Drp1 to alter mitochondrial function in a manner that stimulates synapse formation.
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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.