ArticleCell death & disease2020
Astrocytic BDNF and TrkB regulate severity and neuronal activity in mouse models of temporal lobe epilepsy.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- A meta-analysis of the efficacy of physical exercise interventions on activities of daily living in patients with Alzheimer's disease.Frontiers in public health · 2024Pooled it
- Irisin-BDNF axis mediates muscle-brain communication: a complete molecular cascade and potential bidirectional feedback from peripheral activation to central protection.Biogerontology · 2026Review
- Astrocyte TrkB.T1 Deficiency Disrupts Glutamatergic Synaptogenesis and Astrocyte-Synapse Interactions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Excitatory neurons and astrocytes-specific dysregulation and aberrant interactions are vulnerable to FCDI as suggested by single-cell spatial transcriptomics.Clinical and translational medicine · 2026Article
- Glutamate-induced nuclear translocation of PYK2 in hippocampal neurons, interaction with MBD2, and role in cell death in a model of epilepsy.Cell death & disease · 2026Article
- Review
- Extracellular vesicles derived from astrocytes pretreated with melatonin promoted neuro-angiogenesis in mice with ischemic medial prefrontal cortex.Journal of translational medicine · 2026Article
- Astrocytic Igfbp2 Promotes Spontaneous Seizures in a Mouse Model of Mesial Temporal Lobe Epilepsy.Glia · 2026Article
- The Reparative Mechanisms Underlying Preclinical Neural Stem/Progenitor Cell Therapy for Ischemic Stroke: A Systematic Review.Neurology research international · 2026Review
- Chlorogenic Acid as a Neuroprotective Agent: Enhancing Plasticity and Promoting Brain Health and Functional Reserve.CNS & neurological disorders drug targets · 2026Article
- Article
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- Mammalian TatD DNase domain containing 1 (TATDN1) is a proteostasis-responsive gene with roles in ventricular structure and neuromuscular function.The FEBS journal · 2025Article
- Fenofibrate as a PPARα Agonist Modulates Neuroinflammation and Glutamate Receptors in a Rat Model of Temporal Lobe Epilepsy: Region-Specific Effects and Behavioral Outcomes.International journal of molecular sciences · 2025Article
- IDO Activation Affects BDNF/TrkB Signaling Pathway, Oxidative Stress, and Mitochondrial Enzymatic Activities in Temporal Lobe Epilepsy.Current issues in molecular biology · 2025Article
- Cleavage of the TrkB-FL receptor during epileptogenesis: insights from a kainic acid-induced model of epilepsy and human samples.Pharmacological research · 2025Article
- Optogenetic calcium modulation in astrocytes enhances post-stroke recovery in chronic capsular infarct.Science advances · 2025Article
- Role of Glial Cells and Receptors in Schizophrenia Pathogenesis.Neurochemical research · 2025Review
- Altered Neuroplasticity in Epilepsy is Associated with Neuroinflammation and Oxidative Stress: In vivo Evidence of Brain-Derived Extracellular Vesicles.International journal of nanomedicine · 2025Article
- Functional Remediation Improves Serum BDNF and TrkB Levels in Euthymic Patients with Bipolar Disorder: A Randomized Trial Study.Neuropsychiatric disease and treatment · 2025Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes have emerged as crucial regulators of neuronal network activity, synapse formation, and underlying behavioral and cognitive processes. Despite some pathways have been identified, the communication between astrocytes and neurons remains to be completely elucidated. Unraveling this communication is crucial to design potential treatments for neurological disorders like temporal lobe epilepsy (TLE). The BDNF and TrkB molecules have emerged as very promising therapeutic targets. However, their modulation can be accompanied by several off-target effects such as excitotoxicity in case of uncontrolled upregulation or dementia, amnesia, and other memory disorders in case of downregulation. Here, we show that BDNF and TrkB from astrocytes modulate neuronal dysfunction in TLE models. First, conditional overexpression of BDNF from astrocytes worsened the phenotype in the lithium-pilocarpine mouse model. Our evidences pointed out to the astrocytic pro-BDNF isoform as a major player of this altered phenotype. Conversely, specific genetic deletion of BDNF in astrocytes prevented the increase in the number of firing neurons and the global firing rate in an in vitro model of TLE. Regarding to the TrkB, we generated mice with a genetic deletion of TrkB specifically in hippocampal neurons or astrocytes. Interestingly, both lines displayed neuroprotection in the lithium-pilocarpine model but only the mice with genetic deletion of TrkB in astrocytes showed significantly preserved spatial learning skills. These data identify the astrocytic BDNF and TrkB molecules as promising therapeutic targets for the treatment of TLE.
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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.