ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Differential susceptibility to excitotoxic stress in YAC128 mouse models of Huntington disease between initiation and progression of disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Neuroprotective role of morin hydrate on 3-nitropropionic acid-elicited huntington's disease: in vivo investigation of RIPK1/RIPK3/MLKL necroptosis signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Huntington's Disease: Complex Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington's Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain.Molecules (Basel, Switzerland) · 2023Article
- Early TNF-Dependent Regulation of Excitatory and Inhibitory Synapses on Striatal Direct Pathway Medium Spiny Neurons in the YAC128 Mouse Model of Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Targeting N-type calcium channels in young-onset of some neurological diseases.Frontiers in cell and developmental biology · 2022Review
- C57BL/6 Background Attenuates mHTT Toxicity in the Striatum of YAC128 Mice.International journal of molecular sciences · 2021Article
- Effects of excitotoxicity in the hypothalamus in transgenic mouse models of Huntington disease.Heliyon · 2021Article
- Huntington's disease mouse models: unraveling the pathology caused by CAG repeat expansion.Faculty reviews · 2021Review
- Striatal network modeling in Huntington's Disease.PLoS computational biology · 2020Article
- The Interaction of Aging and Cellular Stress Contributes to Pathogenesis in Mouse and Human Huntington Disease Neurons.Frontiers in aging neuroscience · 2020Article
- DAPK1 Promotes Extrasynaptic GluN2B Phosphorylation and Striatal Spine Instability in the YAC128 Mouse Model of Huntington Disease.Frontiers in cellular neuroscience · 2020Article
- Stress-Sensitive Protein Rac1 and Its Involvement in Neurodevelopmental Disorders.Neural plasticity · 2020Review
- Partial decortication ameliorates dopamine depletion‑induced striatal neuron lesions in rats.International journal of molecular medicine · 2019Article
- Altered Regulation of Striatal NeuronalFrontiers in synaptic neuroscience · 2019Article
- Neurodegenerative diseases: model organisms, pathology and autophagy.Journal of genetics · 2018Review
- Disrupted striatal neuron inputs and outputs in Huntington's disease.CNS neuroscience & therapeutics · 2018Review
- Endocannabinoid-Specific Impairment in Synaptic Plasticity in Striatum of Huntington's Disease Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Differential electrophysiological and morphological alterations of thalamostriatal and corticostriatal projections in the R6/2 mouse model of Huntington's disease.Neurobiology of disease · 2017Article
- SorCS2-mediated NR2A trafficking regulates motor deficits in Huntington's disease.JCI insight · 2017Article
- Postnatal and adult consequences of loss of huntingtin during development: Implications for Huntington's disease.Neurobiology of disease · 2016Article
4 more citing papers are in PubMed but not listed here.
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15 authors.
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Abstract
Huntington disease (HD) is a neurodegenerative disorder caused by an expanded CAG tract in the HD gene. Polyglutamine expansion of huntingtin (htt) results in early, progressive loss of medium spiny striatal neurons, as well as cortical neurons that project to the striatum. Excitotoxicity has been postulated to play a key role in the selective vulnerability of striatal neurons in HD. Early excitotoxic neuropathological changes observed in human HD brain include increased quinolinate (QUIN) concurrent with proliferative changes such as increased spine density and dendritic length. In later stages of the disease, degenerative-type changes are apparent, such as loss of dendritic arborization, a reduction in spine density and reduced levels of 3-hydroxykynurenine and QUIN. It is currently unknown whether sensitivity to excitotoxic stress varies between initiation and progression of disease. Here, we have assessed the excitotoxic phenotype in the YAC128 mouse model of HD by examining the response to excitotoxic stress at different stages of disease. Our results demonstrate that YAC128 mice display enhanced sensitivity to NMDA ex vivo and QUIN in vivo before obvious phenotypic changes. In contrast, 10-month-old symptomatic YAC128 mice are resistant to QUIN-induced neurotoxicity. These findings are paralleled by a significant increase in NMDAR-mediated membrane currents in presymptomatic YAC128 dissociated medium spiny neurons progressing to reduced NMDAR-mediated membrane currents with disease progression. These data highlight the dynamic nature of the mutant htt-mediated excitotoxic phenotype and suggests that therapeutic approaches to HD may need to be altered, depending on the stage and development of the disease.
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