ArticleThe European journal of neuroscience2019
Striatal GABAergic interneuron dysfunction in the Q175 mouse model of Huntington's disease.
Article in The European journal of neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Aberrant medial ganglionic eminence (MGE) GABAergic neurogenesis contributes to Huntington's disease pathogenesis.Neurobiology of disease · 2026Article
- Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.Disease models & mechanisms · 2026Article
- Selective Lis1 inactivation disrupts migration and positioning of cortical somatostatin interneurons.Scientific reports · 2026Article
- From Balance to Breakdown: striatal PV interneurons in Huntington's disease and Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2026Review
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Striatal parvalbumin interneurons are activated in a mouse model of cerebellar dystonia.Disease models & mechanisms · 2024Article
- Transplanted human neural stem cells rescue phenotypes in zQ175 Huntington's disease mice and innervate the striatum.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.Cellular and molecular life sciences : CMLS · 2023Article
- hESC-derived striatal progenitors grafted into a Huntington's disease rat model support long-term functional motor recovery by differentiating, self-organizing and connecting into the lesioned striatum.Stem cell research & therapy · 2023Article
- Editorial: New insight into Huntington's disease: From neuropathology to possible therapeutic targets.Frontiers in neuroscience · 2023Article
- Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons.Life science alliance · 2022Article
- Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Progression of basal ganglia pathology in heterozygous Q175 knock-in Huntington's disease mice.The Journal of comparative neurology · 2021Article
- The difficulty to model Huntington's disease in vitro using striatal medium spiny neurons differentiated from human induced pluripotent stem cells.Scientific reports · 2021Article
- The role of neuropeptide somatostatin in the brain and its application in treating neurological disorders.Experimental & molecular medicine · 2021Review
- BACHD Mice Recapitulate the Striatal Parvalbuminergic Interneuron Loss Found in Huntington's Disease.Frontiers in neuroanatomy · 2021Article
- Age-Dependent Degradation of Locomotion Encoding in Huntington's Disease R6/2 Model Mice.Journal of Huntington's disease · 2021Article
- The Potential Role of Protein Kinase R as a Regulator of Age-Related Neurodegeneration.Frontiers in aging neuroscience · 2021Review
- Striosomes Mediate Value-Based Learning Vulnerable in Age and a Huntington's Disease Model.Cell · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
The pathological hallmark of Huntington's disease (HD) is the massive loss of striatal and cortical neurons. Until recently, it was believed that striatal interneurons were spared from degeneration. This view has changed after the demonstration that parvalbumin (PV)-expressing interneurons also are vulnerable in humans. Here we compared morphological and functional changes of striatal fast-spiking interneurons (FSIs) and low-threshold spiking (LTS) interneurons in the Q175 mouse model of HD at presymptomatic (2 months) and symptomatic (12 months) stages of the disease. Electrophysiological intrinsic and synaptic properties of FSIs were significantly altered in symptomatic mice compared to wild-type (WT) littermates. Overall, FSIs became more excitable with disease progression. Sholl analysis also revealed a significant loss of dendritic complexity and excitatory synaptic inputs. The basic membrane and synaptic properties of LTS interneurons were similar in Q175 and WT mice regardless of disease stage. The resilience of LTS interneurons could be related to their sparsity of excitatory synaptic inputs compared with FSIs. However, in symptomatic mice, a subpopulation of LTS interneurons displayed an increase in action potential firing within oscillating bursts. Thus, we conclude that while both FSI and LTS interneurons demonstrate increases in excitability, the HD mutation differentially affects their membrane and synaptic properties as well as their ability to respond to compensatory challenges presented during the late stage of the disease. Alterations in GABAergic interneuron intrinsic activity and responsiveness to incoming signals may significantly affect SPN output thus contributing to abnormal motor movements in patients afflicted with HD.
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