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| Research article summary (published 10 Feb 2008): |
Time course of choice reaction time deficits in the Hdh(Q92) knock-in mouse model of Huntington's disease in the operant serial implicit learning task (SILT).
Full Abstract
A range of transgenic and knock-in mouse models of Huntington's disease have been created since identification in 1993 of the disease mutation in the HD gene. Knock-in models that express the full-length mutant protein tend to exhibit less severe behavioural deficits than transgenic models and so require more sensitive tasks in order to reveal impairments. To achieve this, we therefore used a Serial Implicit Learning Task (SILT), which measures serial reaction times to visual stimuli, requiring detection and responding in both predictable and unpredictable locations in the 9-hole operant chamber. We have previously reported that knock-in Hdh(Q92/Q92) mice exhibit a modest impairment in learning the SILT tasks at 4 months of age, prior to the formation of overt neuronal nuclear inclusions. In the present study we have explored the time course of the development of impairments from 5 to 14 months of age. The deficit previously found in accuracy and reaction time was present at all ages examined in these Hdh(Q92/Q92) mice; the deficit was not progressive, and did not correlate with the evolution of neuronal nuclear inclusions.
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Author information
Author/s: Trueman, Rebecca C (RC); Brooks, Simon P (SP); Jones, Lesley (L); Dunnett, Stephen B (SB);
Affiliation: School of Biosciences, Cardiff University, Cardiff, Wales, UK. truemanrc(-atsign-)cardiff.ac.uk
Grants: (Agency:United Kingdom Biotechnology and Biological Sciences Research Council) ; (Agency:United Kingdom Medical Research Council)
Journal and publication information
Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
Journal: Behavioural brain research (Behav Brain Res), published in Netherlands. (Language: eng)
Reference: 2008-Jun; vol 189 (issue 2) : pp 317-24
Dates: Created 2008/04/04; Completed 2008/07/09;
PMID: 18367261, status: MEDLINE (last retrieval date: 11/6/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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