Evidence map›Paper›PMID 24348346›Full record

ArticleFrontiers in systems neuroscience2013

Decomposition of abnormal free locomotor behavior in a rat model of Parkinson's disease.

Benjamin Grieb, Constantin von Nicolai, Gerhard Engler, Andrew Sharott, Ismini Papageorgiou, Wolfgang Hamel, Andreas K Engel, Christian K Moll

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

Article in Frontiers in systems neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 17 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Benjamin GriebDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany ; Department of General Psychiatry, Center for Psychosocial Medicine, University of Heidelberg Heidelberg, Germany.
Constantin von NicolaiDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany ; Centre for Integrative Neuroscience, University of Tübingen Tübingen, Germany.
Gerhard EnglerDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany.
Andrew SharottDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany ; Medical Research Council, Anatomical Neuropharacology Unit, Department of Pharmacology, University of Oxford Oxford, UK.
Ismini PapageorgiouDivision of General Neurophysiology, Institute of Physiology and Pathophysiology, University of Heidelberg Heidelberg, Germany.
Wolfgang HamelDepartment of Neurosurgery, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany.
Andreas K EngelDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany.
Christian K MollDepartment of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, University of Hamburg Hamburg, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEBernstein Center for Computational Neuroscience Tübingen · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poverty of spontaneous movement, slowed execution and reduced amplitudes of movement (akinesia, brady- and hypokinesia) are cardinal motor manifestations of Parkinson's disease that can be modeled in experimental animals by brain lesions affecting midbrain dopaminergic neurons. Most behavioral investigations in experimental parkinsonism have employed short-term observation windows to assess motor impairments. We postulated that an analysis of longer-term free exploratory behavior could provide further insights into the complex fine structure of altered locomotor activity in parkinsonian animals. To this end, we video-monitored 23 h of free locomotor behavior and extracted several behavioral measures before and after the expression of a severe parkinsonian phenotype following bilateral 6-hydroxydopamine (6-OHDA) lesions of the rat dopaminergic substantia nigra. Unbiased stereological cell counting verified the degree of midbrain tyrosine hydroxylase positive cell loss in the substantia nigra and ventral tegmental area. In line with previous reports, overall covered distance and maximal motion speed of lesioned animals were found to be significantly reduced compared to controls. Before lesion surgery, exploratory rat behavior exhibited a bimodal distribution of maximal speed values obtained for single movement episodes, corresponding to a "first" and "second gear" of motion. 6-OHDA injections significantly reduced the incidence of second gear motion episodes and also resulted in an abnormal prolongation of these fast motion events. Likewise, the spatial spread of such episodes was increased in 6-OHDA rats. The increase in curvature of motion tracks was increased in both lesioned and control animals. We conclude that the discrimination of distinct modes of motion by statistical decomposition of longer-term spontaneous locomotion provides useful insights into the fine structure of fluctuating motor functions in a rat analog of Parkinson's disease.

Indexed as

6-OHDA lesionsParkinson diseasespontaneous activitystereologyvideo monitoring

Identifiers

PMID24348346
PMCPMC3842038
OpenAlexW2103105123

What OpenQuestion holds

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Registered trials

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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.