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| Research article summary (published 29 Jun 2008): |
A mouse model of fragile X syndrome exhibits heightened arousal and/or emotion following errors or reversal of contingencies.
Full Abstract
This study was designed to further assess cognitive and affective functioning in a mouse model of Fragile X syndrome (FXS), the Fmr1(tm1Cgr) or Fmr1 "knockout" (KO) mouse. Male KO mice and wild-type littermate controls were tested on learning set and reversal learning tasks. The KO mice were not impaired in associative learning, transfer of learning, or reversal learning, based on measures of learning rate. Analyses of videotapes of the reversal learning task revealed that both groups of mice exhibited higher levels of activity and wall-climbing during the initial sessions of the task than during the final sessions, a pattern also seen for trials following an error relative to those following a correct response. Notably, the increase in both behavioral measures seen early in the task was significantly more pronounced for the KO mice than for controls, as was the error-induced increase in activity level. This pattern of effects suggests that the KO mice reacted more strongly than controls to the reversal of contingencies and pronounced drop in reinforcement rate, and to errors in general. This pattern of effects is consistent with the heightened emotional reactivity frequently described for humans with FXS.(c) 2008 Wiley Periodicals, Inc.
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Author information
Author/s: Moon, J (J); Ota, K T (KT); Driscoll, L L (LL); Levitsky, D A (DA); Strupp, B J (BJ);
Affiliation: Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
Grants: HD04024 (Agency:United States NICHD) ; HD047029 (Agency:United States NICHD)
Journal and publication information
Publication Type: Journal Article; Research Support, N.I.H., Extramural
Journal: Developmental psychobiology (Dev Psychobiol), published in United States. (Language: eng)
Reference: 2008-Jul; vol 50 (issue 5) : pp 473-85
Dates: Created 2008/06/18; Completed 2008/08/22;
PMID: 18551464, 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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