Evidence map›Paper›PMID 30782975›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Optogenetic Stimulation of the M2 Cortex Reverts Motor Dysfunction in a Mouse Model of Parkinson's Disease.

Luiz Alexandre Viana Magno, Helia Tenza-Ferrer, Mélcar Collodetti, Matheus Felipe Guimarães Aguiar, Ana Paula Carneiro Rodrigues, Rodrigo Souza da Silva, Joice do Prado Silva, Nycolle Ferreira Nicolau, Daniela Valadão Freitas Rosa, Alexander Birbrair and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  14. Dysfunction of motor cortices in Parkinson's disease.Cerebral cortex (New York, N.Y. : 1991) · 2024
    Review
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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

12 authors at 2 institutions in 1 country.

Luiz Alexandre Viana MagnoCentro de Tecnologia em Medicina Molecular.
Helia Tenza-FerrerCentro de Tecnologia em Medicina Molecular.
Mélcar CollodettiCentro de Tecnologia em Medicina Molecular.
Matheus Felipe Guimarães AguiarCentro de Tecnologia em Medicina Molecular.
Ana Paula Carneiro RodriguesCentro de Tecnologia em Medicina Molecular.
Rodrigo Souza da SilvaCentro de Tecnologia em Medicina Molecular.
Joice do Prado SilvaCentro de Tecnologia em Medicina Molecular.
Nycolle Ferreira NicolauCentro de Tecnologia em Medicina Molecular.
Daniela Valadão Freitas RosaCentro de Tecnologia em Medicina Molecular.
Alexander BirbrairDepartamento de Patologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil 30130-100.
Débora Marques MirandaCentro de Tecnologia em Medicina Molecular.
Marco Aurélio Romano-SilvaCentro de Tecnologia em Medicina Molecular, romano-silva@ufmg.br.
Universidade Federal de Minas Gerais · BRInstituto de Saúde · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuromodulation of deep brain structures (deep brain stimulation) is the current surgical procedure for treatment of Parkinson's disease (PD). Less studied is the stimulation of cortical motor areas to treat PD symptoms, although also known to alleviate motor disturbances in PD. We were able to show that optogenetic activation of secondary (M2) motor cortex improves motor functions in dopamine-depleted male mice. The stimulated M2 cortex harbors glutamatergic pyramidal neurons that project to subcortical structures, critically involved in motor control, and makes synaptic contacts with dopaminergic neurons. Strikingly, optogenetic activation of M2 neurons or axons into the dorsomedial striatum increases striatal levels of dopamine and evokes locomotor activity. We found that dopamine neurotransmission sensitizes the locomotor behavior elicited by activation of M2 neurons. Furthermore, combination of intranigral infusion of glutamatergic antagonists and circuit specific optogenetic stimulation revealed that behavioral response depended on the activity of M2 neurons projecting to SNc. Interestingly, repeated M2 stimulation combined with l-DOPA treatment produced an unanticipated improvement in working memory performance, which was absent in control mice under l-DOPA treatment only. Therefore, the M2-basal ganglia circuit is critical for the assembly of the motor and cognitive function, and this study demonstrates a therapeutic mechanism for cortical stimulation in PD that involves recruitment of long-range glutamatergic projection neurons.

Indexed as

AnimalsDisease Models, AnimalMaleMiceMotor CortexMotor SkillsOptogeneticsOxidopamineParkinson Disease, SecondaryPyramidal CellsTreatment OutcomeOxidopaminebrain stimulationcognitionmovementoptogeneticsParkinson's disorderprefrontal cortex

Identifiers

PMID30782975
PMCPMC6788829
OpenAlexW2917699031

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.