ArticlePloS one2018
Differential changes to D1 and D2 medium spiny neurons in the 12-month-old Q175+/- mouse model of Huntington's Disease.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Mapping brain volume changes in the zQ175DN mouse model of Huntington's disease: a longitudinal MRI study.Biomarker research · 2026Article
- Information flow drives localized morphological differences across neuronal and glial cell types.Frontiers in computational neuroscience · 2026Article
- Restoring endogenous Dlg4/PSD95 expression by an artificial transcription factor ameliorates cognitive and motor learning deficits in the R6/2 mouse model of Huntington's disease.Clinical epigenetics · 2025Article
- Break-up and recovery of harmony between direct and indirect pathways in the basal ganglia: Huntington's disease and treatment.Cognitive neurodynamics · 2024Article
- Cell-Type Specific Regulation of Cholesterogenesis by CYP46A1 Re-Expression in zQ175 HD Mouse Striatum.International journal of molecular sciences · 2023Article
- VGLUT3 Deletion Rescues Motor Deficits and Neuronal Loss in the zQ175 Mouse Model of Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Cholinergic deficits selectively boost cortical intratelencephalic control of striatum in male Huntington's disease model mice.Nature communications · 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
- Synaptic Plasticity Is Predicted by Spatiotemporal Firing Rate Patterns and Robust to In Vivo-like Variability.Biomolecules · 2022Article
- Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Neuronal population models reveal specific linear conductance controllers sufficient to rescue preclinical disease phenotypes.iScience · 2021Article
- Progression of basal ganglia pathology in heterozygous Q175 knock-in Huntington's disease mice.The Journal of comparative neurology · 2021Article
- Kinetic Modelling and Test-Retest Reproducibility for the Dopamine DMolecular imaging and biology · 2021Article
- Early Sensory Deprivation Leads to Differential Inhibitory Changes in the Striatum During Learning.Frontiers in neural circuits · 2021Article
- Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington's Disease.Frontiers in cellular neuroscience · 2021Review
- D1R- and D2R-Medium-Sized Spiny Neurons Diversity: Insights Into Striatal Vulnerability to Huntington's Disease Mutation.Frontiers in cellular neuroscience · 2021Review
- Prediction of Neural Diameter From Morphology to Enable Accurate Simulation.Frontiers in neuroinformatics · 2021Article
- Dopamine Oppositely Modulates State Transitions in Striosome and Matrix Direct Pathway Striatal Spiny Neurons.Neuron · 2020Article
- Striosomes Mediate Value-Based Learning Vulnerable in Age and a Huntington's Disease Model.Cell · 2020Article
- Enhanced GABAergic Inhibition of Cholinergic Interneurons in the zQ175Frontiers in systems neuroscience · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's Disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by deleterious expansion of CAG repeats in the Huntingtin gene and production of neurotoxic mutant Huntingtin protein (mHTT). The key pathological feature of HD is a profound degeneration of the striatum and a loss of cortical volume. The initial loss of indirect pathway (D2) medium spiny neuron (MSN) projections in early stages of HD, followed by a loss of direct pathway (D1) projections in advanced stages has important implications for the trajectory of motor and cognitive dysfunction in HD, but is not yet understood. Mouse models of HD have yielded important information on the effects and mechanisms of mHTT toxicity; however, whether these models recapitulate differential vulnerability of D1 vs. D2 MSNs is unknown. Here, we employed 12-month-old Q175+/- x D2-eGFP mice to examine the detailed structural and functional properties of D1 vs. D2 MSNs. While both D1 and D2 MSNs exhibited increased input resistance, depolarized resting membrane potentials and action potential threshold, only D1 MSNs showed reduced rheobase, action potential amplitude and frequency of spontaneous excitatory postsynaptic currents. Furthermore, D1 but not D2 MSNs showed marked proliferative changes to their dendritic arbors and reductions in spine density. Immunohistochemical assessment showed no loss of glutamatergic afferent inputs from cortical and subcortical sources onto identified D1 and D2 MSNs. Computational models constrained by empirical data predict that the increased dendritic complexity in Q175+/- D1 MSNs likely leads to greater dendritic filtering and attenuation of signals propagating to the soma from the dendrites. Together these findings reveal that, by twelve months, D1 and D2 MSNs exhibit distinctive responses to the presence of mHTT in this important mouse model of HD. This further highlights the need to incorporate findings from D1 and D2 MSNs independently in the context of HD models.
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