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Volume 16, Issue 1, Pages 59-68 (January 2007)


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Short-term social recognition memory deficit and atypical social and physiological stressor reactivity in seizure-susceptible El mice

Chen E. Lim, Laura H. Turner, Stephen C. HeinrichsCorresponding Author Informationemail address

Received 15 August 2006; received in revised form 22 October 2006; accepted 25 October 2006. published online 20 November 2006.

Summary 

The present studies characterize working memory capabilities in the El mouse model of epilepsy using a species-typical social recognition memory task. As the El mouse exhibits a stress hyper-reactivity phenotype, the impact of hypertonic saline consumption, a memory modulatory treatment, upon social recognition performance was also examined. The hypotheses under test were: (1) that seizure susceptible El mice would perform poorly in the short-term working memory task relative to seizure resistant ddY controls, and (2) that the behavioral and neural responses to stressor exposure would be atypical in El mice. Results revealed a short-term working memory deficit and altered reactivity to social, environmental, and physiological stressors in El mice. In Experiment 1, El mice exhibited poor sociability and decreased olfactory investigation times, both anxiogenic-like traits, compared to ddY controls. In Experiment 2, El mice exhibited poor working memory performance compared to capable performance in ddY controls. Social recognition memory in ddY mice was abolished, however, by salt-loading whereas El mice were unaffected by exposure to this physiological stressor. In Experiment 3, all salt-loaded mice exhibited enhanced brain stress neuropeptide (corticotropin releasing factor–CRF) content, and salt-loaded El mice exhibited a 70% reduction in handling-induced seizures. These findings suggest that El mice exhibit high emotionality as well as atypical reactions to stressor exposure, and that these characteristics impact social working memory performance and seizure susceptibility.

Department of Psychology, Boston College, 140 Commonwealth Avenue, Chestnut Hill, MA 02467, USA

Corresponding Author InformationCorresponding author at: VA Boston Medical Center, Research 151 – Neuropharmacology, 150 South Huntington Avenue, Boston, MA 02130-4817, United States. Tel.: +1 857 364 5617.

PII: S1059-1311(06)00199-3

doi:10.1016/j.seizure.2006.10.006


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