Evidence map›Paper›PMID 21677182›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Behavioral and in vivo electrophysiological evidence for presymptomatic alteration of prefrontostriatal processing in the transgenic rat model for huntington disease.

Sophie Höhn, Glenn Dallérac, Alexis Faure, Yvonne K Urbach, Huu Phuc Nguyen, Olaf Riess, Stephan von Hörsten, Pascale Le Blanc, Nathalie Desvignes, Nicole El Massioui and 2 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

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  15. Aberrant calcium signaling by transglutaminase-mediated posttranslational modification of inositol 1,4,5-trisphosphate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2014
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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

12 authors.

Sophie HöhnUniversité Paris-Sud, Centre de Neurosciences Paris-Sud, Unité Mixte de Recherche 8195, F-91405 Orsay, France.
Glenn Dallérac
Alexis Faure
Yvonne K Urbach
Huu Phuc Nguyen
Olaf Riess
Stephan von Hörsten
Pascale Le Blanc
Nathalie Desvignes
Nicole El Massioui
Bruce L Brown
Valerie Doyère

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognitive decline precedes motor symptoms in Huntington disease (HD). A transgenic rat model for HD carrying only 51 CAG repeats recapitulates the late-onset HD phenotype. Here, we assessed prefrontostriatal function in this model through both behavioral and electrophysiological assays. Behavioral examination consisted in a temporal bisection task within a supra-second range (2 vs.8 s), which is thought to involve prefrontostriatal networks. In two independent experiments, the behavioral analysis revealed poorer temporal sensitivity as early as 4 months of age, well before detection of overt motor deficits. At a later symptomatic age, animals were impaired in their temporal discriminative behavior. In vivo recording of field potentials in the dorsomedial striatum evoked by stimulation of the prelimbic cortex were studied in 4- to 5-month-old rats. Input/output curves, paired-pulse function, and plasticity induced by theta-burst stimulation (TBS) were assessed. Results showed an altered plasticity, with higher paired-pulse facilitation, enhanced short-term depression, as well as stronger long-term potentiation after TBS in homozygous transgenic rats. Results from the heterozygous animals mostly fell between wild-type and homozygous transgenic rats. Our results suggest that normal plasticity in prefrontostriatal circuits may be necessary for reliable and precise timing behavior. Furthermore, the present study provides the first behavioral and electrophysiological evidence of a presymptomatic alteration of prefrontostriatal processing in an animal model for Huntington disease and suggests that supra-second timing may be the earliest cognitive dysfunction in HD.

Indexed as

Acoustic StimulationAge FactorsAnalysis of VarianceAnimalsAnimals, Genetically ModifiedBehavior, AnimalCorpus StriatumDiscrimination, PsychologicalDisease Models, AnimalElectric StimulationElectroencephalographyExcitatory Amino Acid AntagonistsGABA AntagonistsGenotypeHuntingtin ProteinHuntington DiseaseExcitatory Amino Acid AntagonistsFG 9041GABA AntagonistsHtt protein, ratHuntingtin ProteinNerve Tissue ProteinsNuclear ProteinsPicrotoxinQuinoxalines

Identifiers

PMID21677182
PMCPMC6622938

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.