Evidence map›Paper›PMID 21978941›Full record

ArticlePharmacology, biochemistry, and behavior2012

Effects of noradrenergic denervation on L-DOPA-induced dyskinesia and its treatment by α- and β-adrenergic receptor antagonists in hemiparkinsonian rats.

Christopher J Barnum, Nirmal Bhide, David Lindenbach, Margaret A Surrena, Adam A Goldenberg, Stefanie Tignor, Anna Klioueva, Hannah Walters, Christopher Bishop

Open access · greenAbstract read
In one paragraph

Article in Pharmacology, biochemistry, and behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 54 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

9 authors at 1 institution in 1 country.

Christopher J BarnumBehavioral Neuroscience Program, Department of Psychology, Binghamton University, Binghamton, NY 13902, USA.
Nirmal Bhide
David Lindenbach
Margaret A Surrena
Adam A Goldenberg
Stefanie Tignor
Anna Klioueva
Hannah Walters
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

While L-3,4-dihydroxyphenylalanine (L-DOPA) remains the standard treatment for Parkinson's disease (PD), long-term efficacy is often compromised by L-DOPA-induced dyskinesia (LID). Recent research suggests that targeting the noradrenergic (NE) system may provide relief from both PD and LID, however, most PD patients exhibit NE loss which may modify response to such strategies. Therefore this investigation aimed to characterize the development and expression of LID and the anti-dyskinetic potential of the α2- and β-adrenergic receptor antagonists idazoxan and propranolol, respectively, in rats receiving 6-OHDA lesions with (DA lesion) or without desipramaine protection (DA+NE lesion). Male Sprague-Dawley rats (N=110) received unilateral 6-hydroxydopamine lesions. Fifty-three rats received desipramine to protect NE neurons (DA lesion) and 57 received no desipramine reducing striatal and hippocampal NE content 64% and 86% respectively. In experiment 1, the development and expression of L-DOPA-induced abnormal involuntary movements (AIMs) and rotations were examined. L-DOPA efficacy using the forepaw adjusting steps (FAS) test was also assessed in DA- and DA+NE-lesioned rats. In experiment 2, DA- and DA+NE-lesioned rats received pre-treatments of idazoxan or propranolol followed by L-DOPA after which the effects of these adrenergic compounds were observed. Results demonstrated that moderate NE loss reduced the development and expression of AIMs and rotations but not L-DOPA efficacy while anti-dyskinetic efficacy of α2- and β-adrenergic receptor blockade was maintained. These findings suggest that the NE system modulates LID and support the continued investigation of adrenergic compounds for the improved treatment of PD.

Indexed as

Adrenergic alpha-AntagonistsAdrenergic beta-AntagonistsAdrenergic NeuronsAnimalsBehavior, AnimalCorpus StriatumDesipramineDisease Models, AnimalDyskinesia, Drug-InducedHippocampusIdazoxanLevodopaMaleMolecular Targeted TherapyNeuroprotective AgentsOxidopamineAdrenergic alpha-AntagonistsAdrenergic beta-AntagonistsDesipramineIdazoxanLevodopaNeuroprotective AgentsOxidopaminePropranolol

Identifiers

PMID21978941
PMCPMC3242909
OpenAlexW1989750506

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.