ArticleNeuron2015
A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase Cγ1 Prevents Epilepsy Induced by Status Epilepticus.
Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 103 citations in OpenAlex.
- Urine-Derived iPSC Neurospheres Uncover Proteomic Correlates of Clinical Severity in Dravet Syndrome.Journal of neurochemistry · 2026Article
- Astrocytic Igfbp2 Promotes Spontaneous Seizures in a Mouse Model of Mesial Temporal Lobe Epilepsy.Glia · 2026Article
- BETMB: A Dual-Target Compound for Synergistic Suppression of Neuronal Hyperexcitability in Refractory Epilepsy via Concurrent Modulation of Nav Channels and GABACNS neuroscience & therapeutics · 2026Article
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- Synaptic accumulation of GluN2B-containing NMDA receptors mediates the effects of BDNF-TrkB signalling on synaptic plasticity and in hyperexcitability during status epilepticus.Journal of biomedical science · 2025Article
- Cleavage of the TrkB-FL receptor during epileptogenesis: insights from a kainic acid-induced model of epilepsy and human samples.Pharmacological research · 2025Article
- Correspondence to "Exploring the impact of exercise induced BDNF on neuroplasticity in neurodegenerative and neuropsychiatric conditions" [Molecular Biology Reports (2025) 52:140].Molecular biology reports · 2025Article
- Activation of hypoactive parvalbumin-positive fast-spiking interneurons restores dentate inhibition to reduce electrographic seizures in the mouse intrahippocampal kainate model of temporal lobe epilepsy.Neurobiology of disease · 2024Article
- New epilepsy therapies in development.Nature reviews. Drug discovery · 2024Review
- Molecular Genetics of Acquired Temporal Lobe Epilepsy.Biomolecules · 2024Review
- The Possible Role of Brain-derived Neurotrophic Factor in Epilepsy.Neurochemical research · 2024Review
- Activation Mechanisms and Diverse Functions of Mammalian Phospholipase C.Biomolecules · 2023Review
- Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- KIF4 regulates neuronal morphology and seizure susceptibility via the PARP1 signaling pathway.The Journal of cell biology · 2023Article
- Insight into Drug Resistance in Status Epilepticus: Evidence from Animal Models.International journal of molecular sciences · 2023Review
- Low-dose 7,8-Dihydroxyflavone Administration After Status Epilepticus Prevents Epilepsy Development.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Chronic partial TrkB activation reduces seizures and mortality in a mouse model of Dravet syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A systems-level analysis highlights microglial activation as a modifying factor in common epilepsies.Neuropathology and applied neurobiology · 2022Article
- Brain-Derived Neurotrophic Factor Inhibits the Function of Cation-Chloride Cotransporter in a Mouse Model of Viral Infection-Induced Epilepsy.Frontiers in cell and developmental biology · 2022Article
- EP2 Antagonists (2011-2021): A Decade's Journey from Discovery to Therapeutics.Journal of medicinal chemistry · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The BDNF receptor tyrosine kinase, TrkB, underlies nervous system function in both health and disease. Excessive activation of TrkB caused by status epilepticus promotes development of temporal lobe epilepsy (TLE), revealing TrkB as a therapeutic target for prevention of TLE. To circumvent undesirable consequences of global inhibition of TrkB signaling, we implemented a novel strategy aimed at selective inhibition of the TrkB-activated signaling pathway responsible for TLE. Our studies of a mouse model reveal that phospholipase Cγ1 (PLCγ1) is the dominant signaling effector by which excessive activation of TrkB promotes epilepsy. We designed a novel peptide (pY816) that uncouples TrkB from PLCγ1. Treatment with pY816 following status epilepticus inhibited TLE and prevented anxiety-like disorder yet preserved neuroprotective effects of endogenous TrkB signaling. We provide proof-of-concept evidence for a novel strategy targeting receptor tyrosine signaling and identify a therapeutic with promise for prevention of TLE caused by status epilepticus in humans.
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