Evidence map›Paper›PMID 30753343›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2019

Motivational Impairment is Accompanied by Corticoaccumbal Dysfunction in the BACHD-Tg5 Rat Model of Huntington's Disease.

Natalie E Zlebnik, Iness Gildish, Thibaut Sesia, Aurelie Fitoussi, Ellen A Cole, Brian P Carson, Roger Cachope, Joseph F Cheer

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

Article in Cerebral cortex (New York, N.Y. : 1991), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 49% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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

8 authors at 2 institutions in 2 countries.

Natalie E ZlebnikDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Iness GildishDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Thibaut SesiaDepartment of Stereotaxy and Functional Neurosurgery, University Hospital of Cologne, Kerpener Str. 62 Cologne, Germany.
Aurelie FitoussiDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Ellen A ColeDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Brian P CarsonDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Roger CachopeDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
Joseph F CheerDepartment of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St., Baltimore, MD, USA.
University of Maryland, Baltimore · USUniversity Hospital Cologne · DE

Funding

Endocannabinoid regulation of corticostriatal network activity in an animal model of cocaine relapseF32DA043967 · NIDA · UNIVERSITY OF MARYLAND BALTIMORE · PI ZLEBNIK, NATALIE · 2018 to 2019
$96k
NIDA NIH HHS F32 DA043967
6 · The paper itself

Abstract

Neuropsychiatric symptoms, such as avolition, apathy, and anhedonia, precede the onset of debilitating motor symptoms in Huntington's disease (HD), and their development may give insight into early disease progression and treatment. However, the neuronal and circuit mechanisms of premanifest HD pathophysiology are not well-understood. Here, using a transgenic rat model expressing the full-length human mutant HD gene, we find early and profound deficits in reward motivation in the absence of gross motor abnormalities. These deficits are accompanied by significant and progressive dysfunction in corticostriatal processing and communication among brain areas critical for reward-driven behavior. Together, our results define early corticostriatal dysfunction as a possible pathogenic contributor to psychiatric disturbances and may help identify potential pharmacotherapeutic targets for the treatment of HD.

Indexed as

RewardAnimalsDisease Models, AnimalHuntingtin ProteinHuntington DiseaseMaleMotivationNeural PathwaysNeuronsNucleus AccumbensOptogeneticsPrefrontal CortexRats, TransgenicHTT protein, humanHuntingtin ProteincorticostriatalHuntington’s diseasemotivationnucleus accumbensprefrontal cortex

Identifiers

PMID30753343
PMCPMC7150618
OpenAlexW2911334679

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.