Optogenetic investigation of neural circuits underlying brain disease in animal models
Identifieur interne : 000056 ( Main/Exploration ); précédent : 000055; suivant : 000057Optogenetic investigation of neural circuits underlying brain disease in animal models
Auteurs : Kay M. Tye [États-Unis] ; Karl Deisseroth [États-Unis]Source :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2012-04.
Abstract
Optogenetic tools have provided a new way to establish causal relationships between brain activity and behaviour in health and disease. Although no animal model captures human disease precisely, behaviours that recapitulate disease symptoms may be elicited and modulated by optogenetic methods, including behaviours that are relevant to anxiety, fear, depression, addiction, autism and parkinsonism. The rapid proliferation of optogenetic reagents together with the swift advancement of strategies for implementation has created new opportunities for causal and precise dissection of the circuits underlying brain diseases in animal models.
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DOI: 10.1038/nrn3171
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Tye</name></author><author><name sortKey="Deisseroth, Karl" sort="Deisseroth, Karl" uniqKey="Deisseroth K" first="Karl" last="Deisseroth">Karl Deisseroth</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E1619554621D8731C5B4FF4800B74A407CD1AA74</idno><date when="2012" year="2012">2012</date><idno type="doi">10.1038/nrn3171</idno><idno type="url">https://api.istex.fr/document/E1619554621D8731C5B4FF4800B74A407CD1AA74/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002B66</idno><idno type="wicri:Area/Main/Curation">002800</idno><idno type="wicri:Area/Main/Exploration">000056</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Optogenetic investigation of neural circuits underlying brain disease in animal models</title><author><name sortKey="Tye, Kay M" sort="Tye, Kay M" uniqKey="Tye K" first="Kay M." last="Tye">Kay M. Tye</name><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Bioengineering, Stanford University, 318 Campus Drive, Clark Center, Stanford, California 94305-5444</wicri:regionArea><wicri:noRegion>California 94305-5444</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Picower Institute of Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139-4307</wicri:regionArea><wicri:noRegion>Massachusetts 02139-4307</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author><author><name sortKey="Deisseroth, Karl" sort="Deisseroth, Karl" uniqKey="Deisseroth K" first="Karl" last="Deisseroth">Karl Deisseroth</name><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Bioengineering, Stanford University, 318 Campus Drive, Clark Center, Stanford, California 94305-5444</wicri:regionArea><wicri:noRegion>California 94305-5444</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Psychiatry, Stanford University, 401 Quarry Road, Stanford, California 94305-5717</wicri:regionArea><wicri:noRegion>California 94305-5717</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>CNC Program, Stanford University, Stanford, California 94305</wicri:regionArea><wicri:noRegion>California 94305</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, Stanford University Medical School, Stanford, California 94305-5323</wicri:regionArea><wicri:noRegion>California 94305-5323</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Nature Reviews Neuroscience</title><idno type="ISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</publisher><date type="published" when="2012-04">2012-04</date><biblScope unit="volume">13</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="251">251</biblScope><biblScope unit="page" to="266">266</biblScope></imprint><idno type="ISSN">1471-003X</idno></series><idno type="istex">E1619554621D8731C5B4FF4800B74A407CD1AA74</idno><idno type="DOI">10.1038/nrn3171</idno><idno type="ArticleID">nrn3171</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1471-003X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Optogenetic tools have provided a new way to establish causal relationships between brain activity and behaviour in health and disease. Although no animal model captures human disease precisely, behaviours that recapitulate disease symptoms may be elicited and modulated by optogenetic methods, including behaviours that are relevant to anxiety, fear, depression, addiction, autism and parkinsonism. The rapid proliferation of optogenetic reagents together with the swift advancement of strategies for implementation has created new opportunities for causal and precise dissection of the circuits underlying brain diseases in animal models.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><country name="États-Unis"><noRegion><name sortKey="Tye, Kay M" sort="Tye, Kay M" uniqKey="Tye K" first="Kay M." last="Tye">Kay M. 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