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JNEUROSCI.2293-20.2020.pdf8.43 MBAdobe PDF見る/開く
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dc.contributor.authorTakakuwa, Norihiroen
dc.contributor.authorIsa, Kaoruen
dc.contributor.authorOnoe, Hirotakaen
dc.contributor.authorTakahashi, Junen
dc.contributor.authorIsa, Tadashien
dc.contributor.alternative高桑, 徳宏ja
dc.contributor.alternative伊佐, かおるja
dc.contributor.alternative尾上, 浩隆ja
dc.contributor.alternative髙橋, 淳ja
dc.contributor.alternative伊佐, 正ja
dc.date.accessioned2022-10-31T01:35:58Z-
dc.date.available2022-10-31T01:35:58Z-
dc.date.issued2021-02-
dc.identifier.urihttp://hdl.handle.net/2433/276953-
dc.description.abstractAfter damage to the primary visual cortex (V1), conscious vision is impaired. However, some patients can respond to visual stimuli presented in their lesion-affected visual field using residual visual pathways bypassing V1. This phenomenon is called "blindsight." Many studies have tried to identify the brain regions responsible for blindsight, and the pulvinar and/or lateral geniculate nucleus (LGN) are suggested to play key roles as the thalamic relay of visual signals. However, there are critical problems regarding these preceding studies in that subjects with different sized lesions and periods of time after lesioning were investigated; furthermore, the ability of blindsight was assessed with different measures. In this study, we used double dissociation to clarify the roles of the pulvinar and LGN by pharmacological inactivation of each region and investigated the effects in a simple task with visually guided saccades (VGSs) using monkeys with a unilateral V1 lesion, by which nearly all of the contralesional visual field was affected. Inactivating either the ipsilesional pulvinar or LGN impaired VGS toward a visual stimulus in the affected field. In contrast, inactivation of the contralesional pulvinar had no clear effect, but inactivation of the contralesional LGN impaired VGS to the intact visual field. These results suggest that the pulvinar and LGN play key roles in performing the simple VGS task after V1 lesioning, and that the visuomotor functions of blindsight monkeys were supported by plastic changes in the visual pathway involving the pulvinar, which emerged after V1 lesioning.SIGNIFICANCE STATEMENT Many studies have been devoted to understanding the mechanism of mysterious symptom called "blindsight, " in which patients with damage to the primary visual cortex (V1) can respond to visual stimuli despite loss of visual awareness. However, there is still a debate on the thalamic relay of visual signals. In this study, to pin down the issue, we tried double dissociation in the same subjects (hemi-blindsight macaque monkeys) and clarified that the lateral geniculate nucleus (LGN) plays a major role in simple visually guided saccades in the intact state, while both pulvinar and LGN critically contribute after the V1 lesioning, suggesting that plasticity in the visual pathway involving the pulvinar underlies the blindsight.en
dc.language.isoeng-
dc.publisherSociety for Neuroscienceen
dc.rightsCopyright © 2021 the authorsen
dc.rightsBeginning six months after publication the Work will be made freely available to the public on SfN’s website to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license. The user may not create, compile, publish, host, enable or otherwise make available a mirror site of The Journal of Neuroscience site.en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subjectblindsighten
dc.subjectlateral geniculate nucleusen
dc.subjectmonkeyen
dc.subjectpulvinaren
dc.subjectsaccadic eye movementen
dc.titleContribution of the Pulvinar and Lateral Geniculate Nucleus to the Control of Visually Guided Saccades in Blindsight Monkeysen
dc.typejournal article-
dc.type.niitypeJournal Article-
dc.identifier.jtitleThe Journal of Neuroscienceen
dc.identifier.volume41-
dc.identifier.issue8-
dc.identifier.spage1755-
dc.identifier.epage1768-
dc.relation.doi10.1523/JNEUROSCI.2293-20.2020-
dc.textversionpublisher-
dc.identifier.pmid33443074-
dcterms.accessRightsopen access-
datacite.awardNumber26221003-
datacite.awardNumber19H01011-
datacite.awardNumber19H05723-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26221003/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-19H01011/-
datacite.awardNumber.urihttps://kaken.nii.ac.jp/grant/KAKENHI-PLANNED-19H05723/-
dc.identifier.pissn0270-6474-
dc.identifier.eissn1529-2401-
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.funderName日本学術振興会ja
jpcoar.awardTitle霊長類の大規模神経回路活動記録・操作法による部分的意識の生成機構の解明ja
jpcoar.awardTitle予測誤差により脊髄損傷後の巧緻運動の機能回復が駆動される神経機構の解明ja
jpcoar.awardTitle生体構造の再構成による超適応機構の解明と潜在適応力低下防止への挑戦ja
出現コレクション:学術雑誌掲載論文等

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