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A role for anterior thalamic nuclei in affective cognition: Interaction with environmental conditions

Authors

  • Alexandra Dupire,

    1. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Talence, France
    2. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), UMR 5287, University of Bordeaux, Talence, France
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  • Patricia Kant,

    1. New Zealand Brain Research Institute, Christchurch, New Zealand
    2. Department of Psychology, University of Canterbury, Christchurch, New Zealand
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  • Nicole Mons,

    1. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Talence, France
    2. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), UMR 5287, University of Bordeaux, Talence, France
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  • Alain R. Marchand,

    1. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Talence, France
    2. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), UMR 5287, University of Bordeaux, Talence, France
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  • Etienne Coutureau,

    1. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Talence, France
    2. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), UMR 5287, University of Bordeaux, Talence, France
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  • John Dalrymple-Alford,

    1. New Zealand Brain Research Institute, Christchurch, New Zealand
    2. Department of Psychology, University of Canterbury, Christchurch, New Zealand
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  • Mathieu Wolff

    Corresponding author
    1. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Talence, France
    2. Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), UMR 5287, University of Bordeaux, Talence, France
    • Institut de Neurosciences Cognitives et Intégratives d'Aquitaines (INCIA), CNRS UMR 5287, Université de Bordeaux 1, Avenue des facultés, Talence, Cedex 33400, France
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Abstract

Damage to anterior thalamic nuclei (ATN) is a well-known cause of diencephalic pathology that produces a range of cognitive deficits reminiscent of a hippocampal syndrome. Anatomical connections of the ATN also extend to cerebral areas that support affective cognition. Enriched environments promote recovery of declarative/relational memory after ATN lesions and are known to downregulate emotional behaviors. Hence, the performance of standard-housed and enriched ATN rats in a range of behavioral tasks engaging affective cognition was compared. ATN rats exhibited reduced anxiety responses in the elevated plus maze, increased activity and reduced corticosterone responses when exploring an open field, and delayed acquisition of a conditioned contextual fear response. ATN rats also exhibited reduced c-Fos and phosphorylated cAMP response element-binding protein (pCREB) immunoreactivity in the hippocampal formation and the amygdala after completion of the contextual fear test. Marked c-Fos hypoactivity and reduced pCREB levels were also evident in the granular retrosplenial cortex and, to a lesser extent, in the anterior cingulate cortex. Unlike standard-housed ATN rats, enriched ATN rats expressed virtually no fear of the conditioned context. These results show that the ATN regulate affective cognition and that damage to this region may produce markedly different behavioral effects as a function of environmental housing conditions. © 2013 Wiley Periodicals, Inc.

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