Evidence map›Paper›PMID 24491966›Full record

ArticleNeurobiology of disease2014

Contributions of signaling by dopamine neurons in dorsal striatum to cognitive behaviors corresponding to those observed in Parkinson's disease.

Martin Darvas, Charles W Henschen, Richard D Palmiter

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
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  4. Establishing the Roles of the Dorsal and Ventral Striatum in Humor Comprehension and Appreciation with fMRI.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  5. Neuroprotective effects of a novel peptide fromFood science & nutrition · 2023
    Article
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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

3 authors at 1 institution in 1 country.

Martin DarvasDepartment of Pathology, University of Washington, Seattle, WA 98195, USA. Electronic address: mdarvas@uw.edu.
Charles W HenschenDepartment of Biochemistry, University of Washington, Seattle, WA 98195, USA.
Richard D PalmiterDepartment of Biochemistry, University of Washington, Seattle, WA 98195, USA; Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.
University of Washington · US

Funding

Udall Center Director's meeting poster awardP50NS062684 · NINDS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2020
$18.3M
NINDS NIH HHS P50 NS062684NINDS NIH HHS P50-NS062684
6 · The paper itself

Abstract

Although the cardinal features of Parkinson's disease (PD) are motor symptoms, PD also causes cognitive deficits including cognitive flexibility and working memory, which are strongly associated with prefrontal cortex (PFC) functions. Yet, early stage PD is not characterized by pathology in the PFC but by a loss of dopaminergic (DA) projections from the substantia nigra to the dorsal striatum. Moreover, the degree to which PD symptoms can be ascribed to the loss of DA alone or to the loss of DA neurons is unknown. We addressed these issues by comparing mouse models of either chronic DA depletion or loss of DA projections to the dorsal striatum. We achieved equal levels of striatal DA reduction in both models which ranged from mild (~25%) to moderate (~60%). Both models displayed DA concentration-dependent reductions of motor function as well as mild deficits of cognitive flexibility and working memory. Interestingly, whereas both motor function and cognitive flexibility were more severely impaired after mild ablation of DA neurons as compared to mild loss of DA alone, both models had equal deficits after moderate loss of DA. Our results confirm contributions of nigro-striatal dopamine signaling to cognitive behaviors that are affected in early stage PD. Furthermore, our findings suggest that the phenotype after ablation of DA neurons accrues from factors beyond the mere loss of DA.

Indexed as

AnimalsCognition DisordersCorpus StriatumDisease Models, AnimalDopamineDopaminergic NeuronsMemoryMiceMice, Inbred C57BLMice, KnockoutMotor ActivityMotor Skills DisordersMuscle StrengthOxidopamineParkinson DiseasePsychomotor PerformanceDopamineOxidopamineSympatholyticsTyrosine 3-Monooxygenase6-HydroxydopamineDopamine-deficient miceExecutive functionNeurodegenerationTyrosine hydroxylaseViral inactivation

Identifiers

PMID24491966
PMCPMC4001780
OpenAlexW2022425735

What OpenQuestion holds

Textmetadata
LicenceTDM
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.