ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Brain-derived neurotrophic factor induces hyperexcitable reentrant circuits in the dentate gyrus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
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- BDNF-DT and BDNF-AS-DT: novel genes in the BDNF locus.Molecular psychiatry · 2026Article
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- The Possible Role of Brain-derived Neurotrophic Factor in Epilepsy.Neurochemical research · 2024Review
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- Molecular mechanisms of exercise intervention in alleviating the symptoms of autism spectrum disorder: Targeting the structural alterations of synapse.Frontiers in psychiatry · 2023Review
- Adenosine AScientific reports · 2022Article
- Genetics and Brain Transcriptomics of Completed Suicide.The American journal of psychiatry · 2022Article
- The potential neuroprotective effects of stingless bee honey.Frontiers in aging neuroscience · 2022Review
- Astrocyte Role in Temporal Lobe Epilepsy and Development of Mossy Fiber Sprouting.Frontiers in cellular neuroscience · 2021Review
- Pathological Targets for Treating Temporal Lobe Epilepsy: Discoveries From Microscale to Macroscale.Frontiers in neurology · 2021Review
- Operation Brain Trauma Therapy: An Exploratory Study of Levetiracetam Treatment Following Mild Traumatic Brain Injury in the Micro Pig.Frontiers in neurology · 2020Article
- Influence of Tacrolimus on Depressive-Like Behavior in Diabetic Rats Through Brain-Derived Neurotrophic Factor Regulation in the Hippocampus.Neurotoxicity research · 2019Article
- The Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and Beyond.International journal of molecular sciences · 2019Review
- KIF2A regulates the development of dentate granule cells and postnatal hippocampal wiring.eLife · 2018Article
- The Molecular and Cellular Mechanisms of Axon Guidance in Mossy Fiber Sprouting.Frontiers in neurology · 2018Review
- Is Mossy Fiber Sprouting a Potential Therapeutic Target for Epilepsy?Frontiers in neurology · 2018Review
- Mechanism of BDNF Modulation in GABAergic Synaptic Transmission in Healthy and Disease Brains.Frontiers in cellular neuroscience · 2018Article
- Hippocampal Pathophysiology: Commonality Shared by Temporal Lobe Epilepsy and Psychiatric Disorders.Neuroscience journal · 2018Review
- The Mechanism of Anti-Epileptogenesis by Levetiracetam Treatment is Similar to the Spontaneous Recovery of Idiopathic Generalized Epilepsy during Adolescence.Psychiatry investigation · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant sprouting and synaptic reorganization of the mossy fiber (MF) axons are commonly found in the hippocampus of temporal lobe epilepsy patients and result in the formation of excitatory feedback loops in the dentate gyrus, a putative cellular basis for recurrent epileptic seizures. Using ex vivo hippocampal cultures, we show that prolonged hyperactivity induces MF sprouting and the resultant network reorganizations and that brain-derived neurotrophic factor (BDNF) is necessary and sufficient to evoke these pathogenic plasticities. Hyperexcitation induced an upregulation of BDNF protein expression in the MF pathway, an effect mediated by L-type Ca2+ channels. The neurotrophin receptor tyrosine kinase (Trk)B inhibitor K252a or function-blocking anti-BDNF antibody prevented hyperactivity-induced MF sprouting. Even under blockade of neural activity, local application of BDNF to the hilus, but not other subregions, was capable of initiating MF axonal remodeling, eventually leading to dentate hyperexcitability. Transfecting granule cells with dominant-negative TrkB prevented axonal branching. Thus, excessive activation of L-type Ca2+ channels causes granule cells to express BDNF, and extracellularly released BDNF stimulates TrkB receptors present on the hilar segment of the MFs to induce axonal branching, which may establish hyperexcitable dentate circuits.
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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.