Evidence map›Paper›PMID 20838211›Full record

ArticleBehavioural pharmacology2010

Behavioral and neurochemical effects of chronic L-DOPA treatment on nonmotor sequelae in the hemiparkinsonian rat.

Karen L Eskow Jaunarajs, Kristin B Dupre, Corinne Y Ostock, Thomas Button, Terrence Deak, Christopher Bishop

Open access · greenAbstract read
In one paragraph

Article in Behavioural pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Neurology international · 2024
    Review
  5. Article
  6. Predictors of dopamine dysregulation syndrome in patients with early Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Article
  7. Article
  8. Olfactory Bulb DToxins · 2022
    Article
  9. Article
  10. Review
  11. The Noradrenergic System in Parkinson's Disease.Frontiers in pharmacology · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Chronic L-dopa decreases serotonin neurons in a subregion of the dorsal raphe nucleus.The Journal of pharmacology and experimental therapeutics · 2014
    Article
  19. Review
  20. 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.

Karen L Eskow JaunarajsBehavioral Neuroscience Program, Department of Psychology, State University of New York at Binghamton, Binghamton, New York, USA.
Kristin B Dupre
Corinne Y Ostock
Thomas Button
Terrence Deak
Christopher Bishop
Binghamton University · US

Funding

Regulation of L-DOPA-induced dyskinesia by 5-HT1A receptor mechanismsR01NS059600 · NINDS · STATE UNIVERSITY OF NY,BINGHAMTON · PI BISHOP, CHRISTOPHER R · 2008 to 2012
$1.3M
NINDS NIH HHS NS059600NINDS NIH HHS R01 NS059600
6 · The paper itself

Abstract

Depression and anxiety are the prevalent nonmotor symptoms that worsen quality of life for Parkinson's disease (PD) patients. Although dopamine (DA) cell loss is a commonly proposed mechanism, the reported efficacy of DA replacement therapy with L-DOPA on affective symptoms is inconsistent. To delineate the effects of DA denervation and chronic L-DOPA treatment on affective behaviors, male Sprague-Dawley rats received unilateral 6-hydroxydopamine or sham lesions and were treated daily with L-DOPA (12 mg/kg+benserazide, 15 mg/kg, subcutaneously) or vehicle (0.9% NaCl, 0.1% ascorbic acid) for 28 days before commencing investigations into anxiety (locomotor chambers, social interaction) and depression-like behaviors (forced swim test) during the OFF phase of L-DOPA. One hour after the final treatments, rats were killed and striatum, prefrontal cortex, hippocampus, and amygdala were analyzed through high-performance liquid chromatography for monoamine levels. In locomotor chambers and social interaction, DA lesions exerted mild anxiogenic effects. Surprisingly, chronic L-DOPA treatment did not improve these effects. Although DA lesion reduced climbing behaviors on day 2 of exposure to the forced swim test, chronic L-DOPA treatment did not reverse these effects. Neurochemically, L-DOPA treatment in hemiparkinsonian rats reduced norepinephrine levels in the prefrontal cortex, striatum, and hippocampus. Collectively, these data suggest that chronic L-DOPA therapy in severely DA-lesioned rats does not improve nonmotor symptoms and may impair nondopaminergic processes, indicating that long-term L-DOPA therapy does not exert necessary neuroplastic changes for improving affect.

Indexed as

AnxietyDepressionDopamine AgentsLevodopaParkinson DiseaseAmygdalaAnimalsBehavioral ResearchBiogenic MonoaminesChromatography, High Pressure LiquidCorpus StriatumDopamineHippocampusHumansMaleModels, AnimalBiogenic MonoaminesDopamineDopamine AgentsLevodopaOxidopamine

Identifiers

PMID20838211
PMCPMC2953710
OpenAlexW1980461727

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.