ArticleJournal of Huntington's disease2013
Striatal synaptosomes from Hdh140Q/140Q knock-in mice have altered protein levels, novel sites of methionine oxidation, and excess glutamate release after stimulation.
Article in Journal of Huntington's disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- Chronic pharmacologic manipulation of dopamine transmission ameliorates metabolic disturbance in Trappc9-linked brain developmental syndrome.JCI insight · 2024Article
- ProteinCoLoc streamlines Bayesian analysis of colocalization in microscopic images.Scientific reports · 2024Article
- Nacc1 Mutation in Mice Models Rare Neurodevelopmental Disorder with Underlying Synaptic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Small-Molecule Disruptors of Mutant Huntingtin-Calmodulin Protein-Protein Interaction Attenuate Deleterious Effects of Mutant Huntingtin.ACS chemical neuroscience · 2022Article
- Huntingtin and Its Partner Huntingtin-Associated Protein 40: Structural and Functional Considerations in Health and Disease.Journal of Huntington's disease · 2022Review
- Inhibition of p38 Mitogen-Activated Protein Kinase Ameliorates HAP40 Depletion-Induced Toxicity and Proteasomal Defect in Huntington's Disease Model.Molecular neurobiology · 2021Article
- Disposition of Proteins and Lipids in Synaptic Membrane Compartments Is Altered in Q175/Q7 Huntington's Disease Mouse Striatum.Frontiers in synaptic neuroscience · 2021Article
- Taming the Huntington's Disease Proteome: What Have We Learned?Journal of Huntington's disease · 2021Review
- Brain sterol flux mediated by cytochrome P450 46A1 affects membrane properties and membrane-dependent processes.Brain communications · 2020Article
- Huntingtin associates with the actin cytoskeleton and α-actinin isoforms to influence stimulus dependent morphology changes.PloS one · 2019Article
- Altered Synaptic Vesicle Release and CaFrontiers in molecular neuroscience · 2018Article
- HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction.Journal of Huntington's disease · 2018Article
- Disruption to schizophrenia-associated gene Fez1 in the hippocampus of HDAC11 knockout mice.Scientific reports · 2017Article
- Differential HspBP1 expression accounts for the greater vulnerability of neurons than astrocytes to misfolded proteins.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Stimulation of synaptoneurosome glutamate release by monomeric and fibrillated α-synuclein.Journal of neuroscience research · 2017Article
- 2,4 DNP improves motor function, preserves medium spiny neuronal identity, and reduces oxidative stress in a mouse model of Huntington's disease.Experimental neurology · 2017Article
- Modulating Neurotrophin Receptor Signaling as a Therapeutic Strategy for Huntington's Disease.Journal of Huntington's disease · 2017Review
- Dysregulation of Corticostriatal Connectivity in Huntington's Disease: A Role for Dopamine Modulation.Journal of Huntington's disease · 2016Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundSynaptic connections are disrupted in patients with Huntington's disease (HD). Synaptosomes from postmortem brain are ideal for synaptic function studies because they are enriched in pre- and post-synaptic proteins important in vesicle fusion, vesicle release, and neurotransmitter receptor activation.
objectiveTo examine striatal synaptosomes from 3, 6 and 12 month old WT and Hdh140Q/140Q knock-in mice for levels of synaptic proteins, methionine oxidation, and glutamate release.
methodsWe used Western blot analysis, glutamate release assays, and liquid chromatography tandem mass spectrometry (LC-MS/MS).
resultsStriatal synaptosomes of 6 month old Hdh140Q/140Q mice had less DARPP32, syntaxin 1 and calmodulin compared to WT. Striatal synaptosomes of 12 month old Hdh140Q/140Q mice had lower levels of DARPP32, alpha actinin, HAP40, Na+/K+-ATPase, PSD95, SNAP-25, TrkA and VAMP1, VGlut1 and VGlut2, increased levels of VAMP2, and modifications in actin and calmodulin compared to WT. More glutamate released from vesicles of depolarized striatal synaptosomes of 6 month old Hdh140Q/140Q than from age matched WT mice but there was no difference in glutamate release in synaptosomes of 3 and 12 month old WT and Hdh140Q/140Q mice. LC-MS/MS of 6 month old Hdh140Q/140Q mice striatal synaptosomes revealed that about 4% of total proteins detected (>600 detected) had novel sites of methionine oxidation including proteins involved with vesicle fusion, trafficking, and neurotransmitter function (synaptophysin, synapsin 2, syntaxin 1, calmodulin, cytoplasmic actin 2, neurofilament, and tubulin). Altered protein levels and novel methionine oxidations were also seen in cortical synaptosomes of 12 month old Hdh140Q/140Q mice.
conclusionsFindings provide support for early synaptic dysfunction in Hdh140Q/140Q knock-in mice arising from altered protein levels, oxidative damage, and impaired glutamate neurotransmission and suggest that study of synaptosomes could be of value for evaluating HD therapies.
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