ArticleFrontiers in systems neuroscience2014
Differential loss of thalamostriatal and corticostriatal input to striatal projection neuron types prior to overt motor symptoms in the Q140 knock-in mouse model of Huntington's disease.
Article in Frontiers in systems neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Thalamic Foxp2 regulates output connectivity and sensory-motor impairments in a model of Huntington's Disease.Cellular and molecular life sciences : CMLS · 2023Article
- Microglia and complement mediate early corticostriatal synapse loss and cognitive dysfunction in Huntington's disease.Nature medicine · 2023Article
- Neurochemical correlates of synapse density in a Huntington's disease mouse model.Journal of neurochemistry · 2023Article
- Cannabinoid signaling and risk in Huntington's disease.Frontiers in computational neuroscience · 2022Article
- Synaptic pathology in Huntington's disease: Beyond the corticostriatal pathway.Neurobiology of disease · 2022Review
- Shedding a new light on Huntington's disease: how blood can both propagate and ameliorate disease pathology.Molecular psychiatry · 2021Article
- Early impairment of thalamocortical circuit activity and coherence in a mouse model of Huntington's disease.Neurobiology of disease · 2021Article
- Progression of basal ganglia pathology in heterozygous Q175 knock-in Huntington's disease mice.The Journal of comparative neurology · 2021Article
- Article
- Striosomes Mediate Value-Based Learning Vulnerable in Age and a Huntington's Disease Model.Cell · 2020Article
- Cortical and Striatal Circuits in Huntington's Disease.Frontiers in neuroscience · 2020Review
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Thinking Outside the Box (and Arrow): Current Themes in Striatal Dysfunction in Movement Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Review
- Cortical Axonal Secretion of BDNF in the Striatum Is Disrupted in the Mutant-huntingtin Knock-in Mouse Model of Huntington's Disease.Experimental neurobiology · 2018Article
- Disrupted striatal neuron inputs and outputs in Huntington's disease.CNS neuroscience & therapeutics · 2018Review
- Effect of early embryonic deletion of huntingtin from pyramidal neurons on the development and long-term survival of neurons in cerebral cortex and striatum.Neurobiology of disease · 2018Article
- Differential changes to D1 and D2 medium spiny neurons in the 12-month-old Q175+/- mouse model of Huntington's Disease.PloS one · 2018Article
- Inflammation alters AMPA-stimulated calcium responses in dorsal striatal D2 but not D1 spiny projection neurons.The European journal of neuroscience · 2017Article
- Generation and Characterization of Knock-in Mouse Models Expressing Versions of Huntingtin with Either an N17 or a Combined PolyQ and Proline-Rich Region Deletion.Journal of Huntington's disease · 2017Article
- Changes in striatal activity and functional connectivity in a mouse model of Huntington's disease.PloS one · 2017Article
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4 authors.
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Abstract
Motor slowing and forebrain white matter loss have been reported in premanifest Huntington's disease (HD) prior to substantial striatal neuron loss. These findings raise the possibility that early motor defects in HD may be related to loss of excitatory input to striatum. In a prior study, we showed that in the heterozygous Q140 knock-in mouse model of HD that loss of thalamostriatal axospinous terminals is evident by 4 months, and loss of corticostriatal axospinous terminals is evident at 12 months, before striatal projection neuron pathology. In the present study, we specifically characterized the loss of thalamostriatal and corticostriatal terminals on direct (dSPN) and indirect (iSPN) pathway striatal projection neurons, using immunolabeling to identify thalamostriatal (VGLUT2+) and corticostriatal (VGLUT1+) axospinous terminals, and D1 receptor immunolabeling to distinguish dSPN (D1+) and iSPN (D1-) synaptic targets. We found that the loss of corticostriatal terminals at 12 months of age was preferential for D1+ spines, and especially involved smaller terminals, presumptively of the intratelencephalically projecting (IT) type. By contrast, indirect pathway D1- spines showed little loss of axospinous terminals at the same age. Thalamostriatal terminal loss was comparable for D1+ and D1- spines at both 4 and 12 months. Regression analysis showed that the loss of VGLUT1+ terminals on D1+ spines was correlated with a slight decline in open field motor parameters at 12 months. Our overall results raise the possibility that differential thalamic and cortical input loss to SPNs is an early event in human HD, with cortical loss to dSPNs in particular contributing to premanifest motor slowing.
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