Evidence map›Paper›PMID 25697958›Full record

ArticleJournal of Parkinson's disease2015

Local Change in Urinary Bladder Contractility Following CNS Dopamine Denervation in the 6-OHDA Rat Model of Parkinson's Disease.

Reinika Mitra, Patrik Aronsson, Michael Winder, Gunnar Tobin, Filip Bergquist, Thomas Carlsson

Open access · hybridAbstract read
In one paragraph

Article in Journal of Parkinson's disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Animal Model for Lower Urinary Tract Dysfunction in Parkinson's Disease.International journal of molecular sciences · 2020
    Review
  6. Autonomic dysfunction in Parkinson disease and animal models.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2019
    Review
  7. Article
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

6 authors at 1 institution in 1 country.

Reinika Mitra
Patrik Aronsson
Michael Winder
Gunnar Tobin
Filip Bergquist
Thomas Carlsson
University of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUrinary problems, including urinary frequency, urgency, and nocturia are some of the non-motor symptoms that correlate most with poor quality of life in Parkinson's disease. However, the mechanism behind these symptoms is poorly understood, in particular regarding peripheral bladder pathophysiology following dopamine degeneration.

objectiveIn this study, we compared the contractile responsiveness of urinary bladder from the 6-OHDA unilateral rat model of Parkinson's disease with that of normal untreated animals.

methodsThe contractility of the urinary detrusor muscle was evaluated in bladder strip preparations using electrical field stimulation, and muscarinic and purinoceptor stimulations in an vitro organ bath setup.

resultsOur data show that the overall contractile response following electrical field stimulation was significantly higher (43% at maximum contraction by 20-40 Hz stimulation) in the 6-OHDA-lesioned rats as compared to control animals. This increase was associated with a significant increase in the cholinergic contractile response, where the muscarinic agonist methacholine produced a 44% (at 10 -4 M concentration) higher response in the 6-OHDA-treated rats as compared to controls with a significant left-shift of the dose response. This indicates an altered sensitivity of the muscarinic receptor system following the specific central 6-OHDA-induced dopamine depletion. In addition a 36% larger contraction of strips from the 6-OHDA animals was also observed with purinoceptor activation using the agonist ATP (5×10 -3 M) during atropine treatment.

conclusionsOur data shows that it is not only the central dopamine control of the micturition reflex that is altered in Parkinson's disease, but also the local contractile function of the urinary bladder. The current study draws attention to a mechanism of urinary dysfunction in Parkinson's disease that has previously not been described.

Indexed as

Adenosine TriphosphateAnimalsCorpus StriatumDenervationDisease Models, AnimalDopaminergic NeuronsElectric StimulationMaleMethacholine ChlorideMuscarinic AgonistsMuscle ContractionOxidopamineParkinsonian DisordersPurinergic AgentsRatsRats, Sprague-DawleyAdenosine TriphosphateMethacholine ChlorideMuscarinic AgonistsOxidopaminePurinergic Agentsdetrusor musclemuscarinic receptorparasympathetic nervous systemUrinary bladder pathophysiology

Identifiers

PMID25697958
PMCPMC4923752
OpenAlexW2271251095

What OpenQuestion holds

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LicenceCC BY-NC
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.