ArticleCellular and molecular life sciences : CMLS2023
Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 5 citations in OpenAlex.
- The potential of vitamins in Huntington's disease: bridging mechanistic evidence with translational limitations and future strategies.Metabolic brain disease · 2026Review
- Comparative analysis of Foxp2 expression in the thalamus of mice, rats, and macaques: implications for the evolution of language circuits.Brain structure & function · 2026Article
- Huntington's disease human lateral ganglionic eminence precursors differentiate into functionally mature medium spiny neurons exhibiting pathology.Stem cells (Dayton, Ohio) · 2026Article
- Fine mapping of PTSD GWAS reveals a role for amygdalabioRxiv : the preprint server for biology · 2026Article
- Hippocampal small RNAs from patients with schizophrenia induce specific cognitive and neural phenotypes in mice.Cell death discovery · 2026Article
- Whole-Genome Resequencing Analysis of Athletic Traits in Grassland-Thoroughbred.Animals : an open access journal from MDPI · 2025Article
- Ubiquitin specific peptidase 11 knockdown slows Huntington's disease progression via regulating mitochondrial dysfunction and neuronal damage depending on PTEN-mediated AKT pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Updated Toolbox for Assessing Neuronal Network Reconstruction after Cell Therapy.Bioengineering (Basel, Switzerland) · 2024Review
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Authors and funding
17 authors at 4 institutions in 2 countries.
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Abstract
backgroundHuntington's Disease (HD) is a disorder that affects body movements. Altered glutamatergic innervation of the striatum is a major hallmark of the disease. Approximately 30% of those glutamatergic inputs come from thalamic nuclei. Foxp2 is a transcription factor involved in cell differentiation and reported low in patients with HD. However, the role of the Foxp2 in the thalamus in HD remains unexplored.
methodsWe used two different mouse models of HD, the R6/1 and the HdhQ111 mice, to demonstrate a consistent thalamic Foxp2 reduction in the context of HD. We used in vivo electrophysiological recordings, microdialysis in behaving mice and rabies virus-based monosynaptic tracing to study thalamo-striatal and thalamo-cortical synaptic connectivity in R6/1 mice. Micro-structural synaptic plasticity was also evaluated in the striatum and cortex of R6/1 mice. We over-expressed Foxp2 in the thalamus of R6/1 mice or reduced Foxp2 in the thalamus of wild type mice to evaluate its role in sensory and motor skills deficiencies, as well as thalamo-striatal and thalamo-cortical connectivity in such mouse models.
resultsHere, we demonstrate in a HD mouse model a clear and early thalamo-striatal aberrant connectivity associated with a reduction of thalamic Foxp2 levels. Recovering thalamic Foxp2 levels in the mouse rescued motor coordination and sensory skills concomitant with an amelioration of neuropathological features and with a repair of the structural and functional connectivity through a restoration of neurotransmitter release. In addition, reduction of thalamic Foxp2 levels in wild type mice induced HD-like phenotypes.
conclusionsIn conclusion, we show that a novel identified thalamic Foxp2 dysregulation alters basal ganglia circuits implicated in the pathophysiology of HD.
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