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Early onset deficits on the delayed alternation task in the HdhQ92 knock-in mouse model of Huntington's disease

Trueman, Rebecca C., Jones, Lesley ORCID: https://orcid.org/0000-0002-3007-4612, Dunnett, Stephen Bruce ORCID: https://orcid.org/0000-0003-1826-1578 and Brooks, Simon Philip ORCID: https://orcid.org/0000-0001-9853-6177 2012. Early onset deficits on the delayed alternation task in the HdhQ92 knock-in mouse model of Huntington's disease. Brain Research Bulletin 88 (2-3) , pp. 156-162. 10.1016/j.brainresbull.2011.03.012

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Abstract

A number of genetic mouse models of Huntington's disease have been created, in order to examine the pathogenesis of Huntington's disease and to test potential therapeutics. In the present study we demonstrate that the full-length knock-in homozygote HdhQ92 mice exhibit impairments at 5 months of age on the delayed alternation task, conducted in 9-hole operant chambers. This test is sensitive to cortico-striatal dysfunction and demonstrates again that although HdhQ92 mice do not display an overt motor phenotype, they do exhibit clear impairments that can be related to deficits seen in HD patients. This indicates that if appropriately sensitive tasks are used, the more subtle and specific HdhQ92 knock-in model could be of use for the examination of pathogenic mechanisms in Huntington's disease and to test potential therapeutics.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Medicine
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords: Huntington’s disease; HdhQ92 mice; Knock-in mice; Operant tests; 9-Hole box; Delayed alternation; Cognitive impairment
Publisher: Elsevier
ISSN: 0361-9230
Last Modified: 11 Mar 2023 02:33
URI: https://orca.cardiff.ac.uk/id/eprint/19497

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