Evidence map›Paper›PMID 30006684›Full record

ArticleNeurotoxicity research2019

Nicotine-Induced Neuroprotection in Rotenone In Vivo and In Vitro Models of Parkinson's Disease: Evidences for the Involvement of the Labile Iron Pool Level as the Underlying Mechanism.

Camila Mouhape, Gustavo Costa, Margot Ferreira, Juan Andrés Abin-Carriquiry, Federico Dajas, Giselle Prunell

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  9. Nicotine-Mediated Rescue of α-Synuclein Toxicity Requires Synaptic Vesicle Glycoprotein 2 in Drosophila.Movement disorders : official journal of the Movement Disorder Society · 2023
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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

6 authors at 1 institution in 1 country.

Camila MouhapeDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay.
Gustavo CostaDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay.
Margot FerreiraDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay.
Juan Andrés Abin-CarriquiryDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay.
Federico DajasDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay.
Giselle PrunellDepartamento de Neuroquímica, Instituto de Investigaciones Biológicas Clemente Estable, Avenida Italia 3318, CP: 11600, Montevideo, Uruguay. gisellefprunell@gmail.com.ORCID http://orcid.org/0000-0002-6412-1114
Instituto de Investigaciones Biológicas Clemente Estable · UY

Funding

Agencia Nacional de Investigación e Innovación FCE2007-517
6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by the degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). Clinical and experimental evidence suggest that the activation of the nicotinic acetylcholine receptor (nAChR) could be protective for PD. In this study, we investigated the neuroprotective capacity of nicotine in a rat PD model. Considering that iron metabolism has been implicated in PD pathophysiology and nicotine has been described to chelate this metal, we also studied the effect of nicotine on the cellular labile iron pool (LIP) levels. Rotenone (1 μg) was unilaterally injected into the median forebrain bundle to induce the degeneration of the nigrostriatal pathway. Nicotine administration (1 mg/K, s.c. daily injection, starting 5 days before rotenone and continuing for 30 days) attenuated the dopaminergic cell loss in the SNpc and the degeneration of the dopaminergic terminals provoked by rotenone, as assessed by immunohistochemistry. Furthermore, nicotine partially prevented the reduction on dopamine levels in the striatum and improved the motor deficits, as determined by HPLC-ED and the forelimb use asymmetry test, respectively. Studies in primary mesencephalic cultures showed that pretreatment with nicotine (50 μM) improved the survival of tyrosine hydroxylase-positive neurons after rotenone (20 nM) exposure. Besides, nicotine induced a reduction in the LIP levels assessed by the calcein dequenching method only at the neuroprotective dose. These effects were prevented by addition of the nAChRs antagonist mecamylamine (100 μM). Overall, we demonstrate a neuroprotective effect of nicotine in a model of PD in rats and that a reduction in iron availability could be an underlying mechanism.

Indexed as

Analysis of VarianceAnimalsCell CountDisease Models, AnimalDopamineDopaminergic NeuronsDose-Response Relationship, DrugEmbryo, MammalianExploratory BehaviorFluoresceinsForelimbInsecticidesIronMaleMedial Forebrain BundleMesencephaloncalcein AMDopamineFluoresceinsInsecticidesIronNicotineNicotinic AgonistsRotenoneTubulinTyrosine 3-MonooxygenaseLabile iron poolNeuroprotectionNicotineParkinson’s diseaseRotenone

Identifiers

PMID30006684
OpenAlexW2884995628

What OpenQuestion holds

Textmetadata
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.