ArticleNature communications2013
BDNF-TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 64 citations in OpenAlex.
- Fingolimod Effects on Motor Function and BDNF-TrkB Signaling in a Huntington's Mouse Model Are Disease-Stage-Dependent.International journal of molecular sciences · 2026Article
- Castration-induced nigrostriatal deficits are linked to reduced TrkB and loss of mature spines in the dorsal striatum.Frontiers in endocrinology · 2026Article
- Sexually Dimorphic Cellular Architecture and Neural Circuity of ovBNST Proenkephalin Neurons.Neuroscience bulletin · 2025Article
- Impaired striatal glutathione-ascorbate metabolism induces transient dopamine increase and motor dysfunction.Nature metabolism · 2024Article
- TrkB signalling regulates dopamine circuits and motor function through metabolic pathways.Nature metabolism · 2024Article
- Ablation of TrkB from Enkephalinergic Precursor-Derived Cerebellar Granule Cells Generates Ataxia.Biology · 2024Article
- BDNF-Regulated Modulation of Striatal Circuits and Implications for Parkinson's Disease and Dystonia.Biomedicines · 2024Review
- A P2RY12 deficiency results in sex-specific cellular perturbations and sexually dimorphic behavioral anomalies.Journal of neuroinflammation · 2024Article
- Preserved VPS13A distribution and expression in Huntington's disease: divergent mechanisms of action for similar movement disorders?Frontiers in neuroscience · 2024Article
- Intensive exercise ameliorates motor and cognitive symptoms in experimental Parkinson's disease restoring striatal synaptic plasticity.Science advances · 2023Article
- Article
- Individual differences and knockout in zebrafish reveal similar cognitive effects of BDNF between teleosts and mammals.Proceedings. Biological sciences · 2022Article
- Individual differences in stereotypy and neuron subtype translatome with TrkB deletion.Molecular psychiatry · 2021Article
- Future Portrait of the Athletic Brain: Mechanistic Understanding of Human Sport PerformanceFrontiers in systems neuroscience · 2020Article
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration.International journal of molecular sciences · 2019Review
- Postnatal TrkB ablation in corticolimbic interneurons induces social dominance in male mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- ERK/MAPK Signaling Is Required for Pathway-Specific Striatal Motor Functions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Modulating Neurotrophin Receptor Signaling as a Therapeutic Strategy for Huntington's Disease.Journal of Huntington's disease · 2017Review
- Upregulation of brain-derived neurotrophic factor in advanced gastric cancer contributes to bone metastatic osteolysis by inducing long pentraxin 3.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The physiology of brain-derived neurotrophic factor signaling in enkephalinergic striatopallidal neurons is poorly understood. Changes in cortical Bdnf expression levels, and/or impairment in brain-derived neurotrophic factor anterograde transport induced by mutant huntingtin (mHdh) are believed to cause striatopallidal neuron vulnerability in early-stage Huntington's disease. Although several studies have confirmed a link between altered cortical brain-derived neurotrophic factor signaling and striatal vulnerability, it is not known whether the effects are mediated via the brain-derived neurotrophic factor receptor TrkB, and whether they are direct or indirect. Using a novel genetic mouse model, here, we show that selective removal of brain-derived neurotrophic factor-TrkB signaling from enkephalinergic striatal targets unexpectedly leads to spontaneous and drug-induced hyperlocomotion. This is associated with dopamine D2 receptor-dependent increased striatal protein kinase C and MAP kinase activation, resulting in altered intrinsic activation of striatal enkephalinergic neurons. Therefore, brain-derived neurotrophic factor/TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior by modulating neuronal activity in response to excitatory input through the protein kinase C/MAP kinase pathway.
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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.