ArticleCNS neuroscience & therapeutics2018
Neurotrophin-3 restores synaptic plasticity in the striatum of a mouse model of Huntington's disease.
Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 31 citations in OpenAlex.
- Theta-shaking mitigates cognitive-emotional decline via subiculum and ventral septum metabolic plasticity.Mechanobiology in medicine · 2025Article
- Human striatal progenitor cells that contain inducible safeguards and overexpress BDNF rescue Huntington's disease phenotypes.Molecular therapy. Methods & clinical development · 2025Article
- Phytochemicals Targeting BDNF Signaling for Treating Neurological Disorders.Brain sciences · 2025Review
- BDNF augmentation reverses cranial radiation therapy-induced cognitive decline and neurodegenerative consequences.Acta neuropathologica communications · 2024Article
- Long non-coding RNA CASC15 enhances learning and memory in mice by promoting synaptic plasticity in hippocampal neurons.Exploration (Beijing, China) · 2024Article
- NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Neurotrophin-3 Rescues Striatal Synaptic Plasticity in Model of Neurodegeneration by PLC Signaling Activation.CNS & neurological disorders drug targets · 2024Article
- Dysregulation of Synaptic Plasticity Markers in Schizophrenia.Indian journal of clinical biochemistry : IJCB · 2023Review
- Neuroprotective effects of Neurotrophin-3 in MPTP-induced zebrafish Parkinson's disease model.Frontiers in pharmacology · 2023Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- The Role of the Second Extracellular Loop of Norepinephrine Transporter, Neurotrophin-3 and Tropomyosin Receptor Kinase C in T Cells: A Peripheral Biomarker in the Etiology of Schizophrenia.International journal of molecular sciences · 2021Article
- Molecular Regulatory Mechanism and Toxicology of Neurodegenerative Processes in MPTP/Probenecid-Induced Progressive Parkinson's Disease Mice Model Revealed by Transcriptome.Molecular neurobiology · 2021Article
- Neuronal Plasticity: Neuronal Organization is Associated with Neurological Disorders.Journal of molecular neuroscience : MN · 2020Review
- Tolfenamic Acid Attenuates 3-Nitropropionic Acid-Induced Biochemical Alteration in Mice.Neurochemical research · 2018Article
- Huntington's disease: From basic science to therapeutics.CNS neuroscience & therapeutics · 2018Article
- Neurotrophin-3 restores synaptic plasticity in the striatum of a mouse model of Huntington's disease.CNS neuroscience & therapeutics · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsNeurotrophin-3 (NT-3) is expressed in the mouse striatum; however, it is not clear the NT-3 role in striatal physiology. The expression levels of mRNAs and immune localization of the NT-3 protein and its receptor TrkC are altered in the striatum following damage induced by an in vivo treatment with 3-nitropropionic acid (3-NP), a mitochondrial toxin used to mimic the histopathological hallmarks of Huntington's disease (HD). The aim of this study was to evaluate the role of NT-3 on corticostriatal synaptic transmission and its plasticity in both the control and damaged striatum.
methodsCorticostriatal population spikes were electrophysiologically recorded and striatal synaptic plasticity was induced by high-frequency stimulation. Further, the phosphorylation status of Trk receptors was tested under conditions that imitated electrophysiological experiments.
resultsNT-3 modulates both synaptic transmission and plasticity in the striatum; nonetheless, synaptic plasticity was modified by the 3-NP treatment, where instead of producing striatal long-term depression (LTD), long-term potentiation (LTP) was obtained. Moreover, the administration of NT-3 in the recording bath restored the plasticity observed under control conditions (LTD) in this model of striatal degeneration.
conclusionNT-3 modulates corticostriatal transmission through TrkB stimulation and restores striatal LTD by signaling through its TrkC receptor.
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