Publication:
Temporal control deficits in murine models of Huntington's disease

dc.contributor.coauthorBrunner, Dani
dc.contributor.coauthorCurtin, Paul C.P.
dc.contributor.coauthorFarrar, Andrew
dc.contributor.coauthorOakeshott, Steve
dc.contributor.coauthorSutphen, Jane
dc.contributor.coauthorBerger, Jason
dc.contributor.coauthorHowland, David
dc.contributor.departmentDepartment of Psychology
dc.contributor.kuauthorBalcı, Fuat
dc.contributor.schoolcollegeinstituteCollege of Social Sciences and Humanities
dc.date.accessioned2024-11-09T23:53:20Z
dc.date.issued2015
dc.description.abstractTiming is a ubiquitous process that underlies a great variety of human activities and depends on highly conserved neuronal circuitry, the cortico-striatal loops. The peak interval (PI) task is an operant task that conditions subjects to initiate and terminate behavioral responses bracketing a fixed interval associated with reinforcement. Performance in this task depends on the efficacy of temporal control processes that coordinate interval encoding and decoding, instrumental response innitiation, cessation and maintenance, and motor control. Here, we used the PI procedure to characterize temporal control in zQ175 knockin (KI) and BAC HD transgenic (Tg) mice generated to model Huntington's Disease (HD), and contrast the result with previously published R6/2 Tg PI data. HD is a progressive neurodegenerative disorder that involves degeneration of the same neural circuits underlying temporal information processing and control of motor output. Our results indicate that temporal control is disrupted in R6/2 Tg and zQ175 KI mice but intact in BAC HD Tg mice. Trial-by-trial analysis of break-run patterns in response rates indicated that shifts in zQ175 KI response curves were driven by significant delays in response initiation and cessation. Similar temporal control deficits were previously reported in HD patients and R6/2 transgenic HD mice. These findings support the use of zQ175 mice in preclinical studies of HD-related cognitive deficits. They provide evidence of a strong homology between the human and rodent neural bases of temporal information processing, temporal response control, and their pathology in neurodegeneration.
dc.description.indexedbyScopus
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.volume28
dc.identifier.issn0889-3667
dc.identifier.linkhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85053258110andpartnerID=40andmd5=197eabdb7ed4191a2775f03efb4e5f51
dc.identifier.quartileN/A
dc.identifier.scopus2-s2.0-85053258110
dc.identifier.urihttps://escholarship.org/uc/item/1751272k
dc.identifier.urihttps://hdl.handle.net/20.500.14288/14996
dc.keywordsInterval timing
dc.keywordsTime perception
dc.keywordsYoung adult
dc.language.isoeng
dc.publisherThe Regents of the University of California
dc.relation.ispartofInternational Journal of Comparative Psychology
dc.subjectPsychology
dc.titleTemporal control deficits in murine models of Huntington's disease
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorBalcı, Fuat
local.publication.orgunit1College of Social Sciences and Humanities
local.publication.orgunit2Department of Psychology
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