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

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dc.creatorLuiz Alexandre Viana Magno
dc.creatorAlexander Birbrair
dc.creatorDébora Marques Miranda
dc.creatorMarco Aurélio Romano-silva
dc.creatorHelia Tenza-ferrer
dc.creatorMélcar Collodetti
dc.creatorMatheus Felipe Guimarães Aguiar
dc.creatorAna Paula Carneiro Rodrigues
dc.creatorRodrigo Souza da Silva
dc.creatorJoice do Prado Silva
dc.creatorNycolle Ferreira Nicolau
dc.creatorDaniela Valadão Freitas Rosa
dc.date.accessioned2023-07-18T20:23:17Z
dc.date.accessioned2025-09-09T00:54:11Z
dc.date.available2023-07-18T20:23:17Z
dc.date.issued2019-04-24
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1523/JNEUROSCI.2277-18.2019
dc.identifier.issn0270-6474
dc.identifier.urihttps://hdl.handle.net/1843/56636
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofThe Journal of Neuroscience
dc.rightsAcesso Aberto
dc.subjectEncéfalo
dc.subjectCognição
dc.subjectMovimento
dc.subjectOptogenética
dc.subjectCórtex Pré-Frontal
dc.subject.otherBrain stimulation
dc.subject.otherCognition
dc.subject.otherMovement
dc.subject.otherOptogenetics
dc.subject.otherParkinson’s disorder
dc.subject.otherPrefrontal cortex
dc.titleOptogenetic Stimulation of the M2 Cortex Reverts Motor Dysfunction in a Mouse Model of Parkinson’s Disease
dc.typeArtigo de periódico
local.citation.epage3248
local.citation.issue17
local.citation.spage3234
local.citation.volume39
local.description.resumoNeuromodulation of deep brain structures (deep brain stimulation)isthe current surgical procedurefortreatment 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 ableto showthat optogenetic activation of secondary (M2) motor cortex improves motorfunctions in dopamine-depleted male mice. The stimulated M2 cortex harbors glutamatergic pyramidal neurons that project to subcortical structures, critically involved inmotor control, andmakes synaptic contactswithdopaminergic neurons. Strikingly, optogenetic activation ofM2 neurons or axonsinto 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.
local.identifier.orcidhttps://orcid.org/0000-0002-7081-8401
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIA
local.publisher.departmentICB - INSTITUTO DE CIÊNCIAS BIOLOGICAS
local.publisher.departmentMED - DEPARTAMENTO DE PEDIATRIA
local.publisher.initialsUFMG
local.url.externahttps://www.jneurosci.org/content/39/17/3234

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