ArticleNeuroscience letters2012
Abnormal burst patterns of single neurons recorded in the substantia nigra reticulata of behaving 140 CAG Huntington's disease mice.
Article in Neuroscience letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Synaptic pathology in Huntington's disease: Beyond the corticostriatal pathway.Neurobiology of disease · 2022Review
- Dysregulation of Corticostriatal Connectivity in Huntington's Disease: A Role for Dopamine Modulation.Journal of Huntington's disease · 2016Review
- Use of a force-sensing automated open field apparatus in a longitudinal study of multiple behavioral deficits in CAG140 Huntington's disease model mice.Behavioural brain research · 2015Article
- Dopamine Receptors and Neurodegeneration.Aging and disease · 2015Review
- Abnormal Bursting as a Pathophysiological Mechanism in Parkinson's Disease.Basal ganglia · 2014Article
- Article
- Dysregulation of corticostriatal ascorbate release and glutamate uptake in transgenic models of Huntington's disease.Antioxidants & redox signaling · 2013Article
- Multiple sources of striatal inhibition are differentially affected in Huntington's disease mouse models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Huntington's disease (HD) is an inherited neurodegenerative disorder that causes neurological pathology in the basal ganglia and related circuitry. A key site of HD pathology is striatum, the principal basal ganglia input structure; striatal pathology likely changes basal ganglia output but no existing studies address this issue. In this report, we characterize single-neuron activity in the substantia nigra reticulata (SNr) of awake, freely behaving 140 CAG knock-in (KI) mice at 16-40 weeks. KI mice are a well characterized model of adult HD and are mildly symptomatic in this age range. As the primary basal ganglia output nucleus in rodents, the SNr receives direct innervation from striatum, as well as indirect influence via polysynaptic inputs. We analyzed 32 single neurons recorded from KI animals and 44 from wild-type (WT) controls. We found increased burst rates, without a concordant change in spike discharge rate, in KI animals relative to WTs. Furthermore, although metrics of burst structure, such as the inter-spike interval in bursts, do not differ between groups, burst rate increases with age in KI, but not WT, animals. Our findings suggest that altered basal ganglia output is a physiological feature of early HD pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.