Evidence map›Paper›PMID 25762686›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Cortical efferents lacking mutant huntingtin improve striatal neuronal activity and behavior in a conditional mouse model of Huntington's disease.

Ana María Estrada-Sánchez, Courtney L Burroughs, Stephen Cavaliere, Scott J Barton, Shirley Chen, X William Yang, George V Rebec

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 59 citations in OpenAlex.

  1. Pathomechanisms of behavioral abnormalities in Huntington disease: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  2. Article
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  6. Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Striatal network modeling in Huntington's Disease.PLoS computational biology · 2020
    Article
  14. Article
  15. Review
  16. 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 · 2019
    Review
  17. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Ana María Estrada-SánchezProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and.ORCID http://orcid.org/0000-0002-7191-4446
Courtney L BurroughsProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and.
Stephen CavaliereProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and.
Scott J BartonProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and.
Shirley ChenProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and.
X William YangCenter for Neurobehavioral Genetics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095.
George V RebecProgram in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405, and rebec@indiana.edu.
Indiana University Bloomington · USUniversity of California, Los Angeles · US

Funding

Conditional Mouse Models: Non-cell-antonomous Toxicities in Huntington's DiseaseR01NS049501 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2004 to 2014
$3.8M
Complement-Microglia Interaction in Synaptic Loss and Neurodegeneration in HDR01NS084298 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI STEVENS, BETH ANN, YANG, XIANGDONG WILLIAM · 2014 to 2018
$1.8M
Validating NT17 Dependent Mechanisms in Huntington's Disease SuppressionR01NS074312 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2011 to 2014
$1.4M
NINDS NIH HHS R01 NS049501NINDS NIH HHS R01NS049501NINDS NIH HHS R01 NS074312NINDS NIH HHS R01NS074312NINDS NIH HHS R01 NS084298
6 · The paper itself

Abstract

Abnormal electrophysiological activity in the striatum, which receives dense innervation from the cerebral cortex, is believed to set the stage for the behavioral phenotype observed in Huntington's disease (HD), a neurodegenerative condition caused by mutation of the huntingtin (mhtt) protein. However, cortical involvement is far from clear. To determine whether abnormal striatal processing can be explained by mhtt alone (cell-autonomous model) or by mhtt in the corticostriatal projection cell-cell interaction model, we used BACHD/Emx1-Cre (BE) mice, a conditional HD model in which full-length mhtt is genetically reduced in cortical output neurons, including those that project to the striatum. Animals were assessed beginning at 20 weeks of age for at least the next 40 weeks, a range over which presymptomatic BACHD mice become symptomatic. Both open-field and nest-building behavior deteriorated progressively in BACHD mice relative to both BE and wild-type (WT) mice. Neuronal activity patterns in the dorsal striatum, which receives input from the primary motor cortex (M1), followed a similar age progression because BACHD activity changed more rapidly than either BE or WT mice. However, in the M1, BE neuronal activity differed significantly from both WT and BACHD. Although abnormal cortical activity in BE mice likely reflects input from mhtt-expressing afferents, including cortical interneurons, improvements in BE striatal activity and behavior suggest a critical role for mhtt in cortical output neurons in shaping the onset and progression of striatal dysfunction.

Indexed as

Huntington DiseaseAction PotentialsAnimalsBrain WavesCerebral CortexConditioning, PsychologicalCorpus StriatumDisease Models, AnimalEfferent PathwaysEmpty Spiracles Homeobox ProteinsExploratory BehaviorFemaleHomeodomain ProteinsHuntingtin ProteinLearning DisabilitiesMaleEmpty Spiracles Homeobox ProteinsHomeodomain ProteinsHtt protein, mouseHuntingtin ProteinNerve Tissue ProteinsNuclear ProteinsTranscription FactorsBAC-CreBACHD miceHuntington's diseasein vivo electrophysiologymotor cortexstriatum

Identifiers

PMID25762686
PMCPMC4355206
OpenAlexW1973877095

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.