ArticleNeuron2014
Impaired TrkB receptor signaling underlies corticostriatal dysfunction in Huntington's disease.
Article in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed.
- Beyond total BDNF: The proBDNF/mBDNF balance in substance use disorders.Neurobiology of disease · 2026Review
- Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity.bioRxiv : the preprint server for biology · 2026Article
- Neurotrophins and Galectin-3: Hidden Keys in Neuroinflammation-A Narrative Review.International journal of molecular sciences · 2026Review
- Synaptic aging and neurodegeneration: the role of synaptic vesicle dynamics and neurotransmitter imbalance.Biogerontology · 2026Review
- Vitamin C Transport Deficiency Alters Striatal Dopamine Gene Expression and Metabolism in YAC128 Huntington Disease Mice.Genes, brain, and behavior · 2025Article
- Upregulation of endocannabinoid signaling in vivo restores striatal synaptic plasticity and motor performance in Huntington's disease mice.Journal of Huntington's disease · 2025Article
- AMPA receptor diffusional trapping machinery as an early therapeutic target in neurodegenerative and neuropsychiatric disorders.Translational neurodegeneration · 2025Review
- Brain-Derived Neurotrophic Factor (BDNF) in Huntington's Disease: Neurobiology and Therapeutic Potential.Current neuropharmacology · 2025Review
- Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- BDNF and TRiC-inspired reagent rescue cortical synaptic deficits in a mouse model of Huntington's disease.Neurobiology of disease · 2024Article
- Age- and region-dependent cortical excitability in the zQ175 Huntington disease mouse model.Human molecular genetics · 2024Article
- Rapid and high-purity differentiation of human medium spiny neurons reveals LMNB1 hypofunction and subtype necessity in modeling Huntington's disease.Inflammation and regeneration · 2024Article
- Transplanted human neural stem cells rescue phenotypes in zQ175 Huntington's disease mice and innervate the striatum.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Distributed dopaminergic signaling in the basal ganglia and its relationship to motor disability in Parkinson's disease.Current opinion in neurobiology · 2023Review
- Neuroprotective effects of hepatoma-derived growth factor in models of Huntington's disease.Life science alliance · 2023Article
- Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington's disease.Nature medicine · 2023Article
- Dopaminergic Input Regulates the Sensitivity of Indirect Pathway Striatal Spiny Neurons to Brain-Derived Neurotrophic Factor.Biology · 2023Article
- The NONRATT023402.2/rno-miR-3065-5p/NGFR axis affects levodopa-induced dyskinesia in a rat model of Parkinson's disease.Cell death discovery · 2023Article
- Brain-Derived Neurotrophic Factor Dysregulation as an Essential Pathological Feature in Huntington's Disease: Mechanisms and Potential Therapeutics.Biomedicines · 2023Review
58 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors.
Funding
Abstract
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder. The debilitating choreic movements that plague HD patients have been attributed to striatal degeneration induced by the loss of cortically supplied brain-derived neurotrophic factor (BDNF). Here, we show that in mouse models of early symptomatic HD, BDNF delivery to the striatum and its activation of tyrosine-related kinase B (TrkB) receptors were normal. However, in striatal neurons responsible for movement suppression, TrkB receptors failed to properly engage postsynaptic signaling mechanisms controlling the induction of potentiation at corticostriatal synapses. Plasticity was rescued by inhibiting p75 neurotrophin receptor (p75NTR) signaling or its downstream target phosphatase-and-tensin-homolog-deleted-on-chromosome-10 (PTEN). Thus, corticostriatal synaptic dysfunction early in HD is attributable to a correctable defect in the response to BDNF, not its delivery.
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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.