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Lack of mutant huntingtin in cortical efferents improves behavioral inflexibility and corticostriatal dynamics in Huntington´s disease mice

dc.contributor.authorEstrada Sánchez, Ana María
dc.contributor.authorBlake, Courtney L.
dc.contributor.authorBarton, Scott J.
dc.contributor.authorHowe, Andrew G.
dc.contributor.authorRebec, George V.
dc.date.accessioned2021-02-06T00:48:18Z
dc.date.available2021-02-06T00:48:18Z
dc.date.issued2019
dc.identifier.citationLack of mutant huntingtin in cortical efferents improves behavioral inflexibility and corticostriatal dynamics in Huntington´s disease mice Ana María Estrada-Sánchez, Courtney L. Blake, Scott J. Barton, Andrew G. Howe, and George V. Rebec Journal of Neurophysiology 2019 122:6, 2621-2629
dc.identifier.urihttp://hdl.handle.net/11627/5531
dc.description.abstract"Abnormal communication between cerebral cortex and striatum plays a major role in the motor symptoms of Huntington’s disease (HD), a neurodegenerative disorder caused by a mutation of the huntingtin gene (mHTT). Because cortex is the main driver of striatal processing, we recorded local field potential (LFP) activity simultaneously in primary motor cortex (M1) and dorsal striatum (DS) in BACHD mice, a full-length HD gene model, and in a conditional BACHD/Emx-1 Cre (BE) model in which mHTT is suppressed in cortical efferents, while mice freely explored a plus-shaped maze beginning at 20 wk of age. Relative to wild-type (WT) controls, BACHD mice were just as active across >40 wk of testing but became progressively less likely to turn into a perpendicular arm as they approached the choice point of the maze, a sign of HD motor inflexibility. BE mice, in contrast, turned as freely as WT throughout testing. Although BE mice did not exactly match WT in LFP activity, the reduction in alpha (8–13 Hz), beta (13–30 Hz), and low-gamma (30–50 Hz) power that occurred in M1 of turning-impaired BACHD mice was reversed. No reversal occurred in DS. In fact, BE mice showed further reductions in DS theta (4–8 Hz), beta, and low-gamma power relative to the BACHD model. Coherence analysis indicated a dysregulation of corticostriatal information flow in both BACHD and BE mice. Collectively, our results suggest that mHTT in cortical outputs drives the dysregulation of select cortical frequencies that accompany the loss of behavioral flexibility in HD."
dc.publisherThe American Physiological Society.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectBACHD mice
dc.subjectDorsal striatum
dc.subjectLocal field potentials
dc.subjectM1 cortex
dc.subjectMotor inflexibility
dc.subject.classificationNEUROCIENCIAS
dc.titleLack of mutant huntingtin in cortical efferents improves behavioral inflexibility and corticostriatal dynamics in Huntington´s disease mice
dc.typearticle
dc.identifier.doihttps://doi.org/10.1152/jn.00777.2018
dc.rights.accessAcceso Abierto


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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