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Mice lacking the cell adhesion molecule Thy-1 fail to use socially transmitted cues to direct their choice of food

  1. Author:
    Mayeux-Portas, V.
    File, S. E.
    Stewart, C. L.
    Morris, R. J.
  2. Author Address

    Morris RJ GKT Med Sch, Mol Neurobiol Grp Guys Campus London SE1 1UL England GKT Med Sch, Mol Neurobiol Grp London SE1 1UL England GKT Sch Biomed Sci, Psychopharmacol Res Unit London SE1 1UL England NCI, Frederick Canc Res & Dev Ctr, Lab Canc & Dev Biol Frederick, MD 21710 USA
    1. Year: 2000
  1. Journal: Current Biology
    1. 10
    2. 2
    3. Pages: 68-75
  2. Type of Article: Article
  1. Abstract:

    Background: Thy-1 is a major cell-surface glycoprotein of mature neurons and certain other cells, including those of the lymphoreticular system. Despite being the simplest member of the immunoglobulin superfamily, the biological role of Thy-1 has proved elusive. Analysis of Thy-1 null mice has shown the presence of excessive GABAergic inhibition of neurotransmission in the dentate gyrus of the hippocampal formation selectively, without any neurological or behavioural effects being apparent. Results: We show here that Thy-1 null mice are unable to make the appropriate dietary choice in the test for social transmission of food preference, despite showing a normal level of social interaction with the demonstrator mouse, normal neophobia, and normal learning in a T-maze using scented food as cues. The mice also performed normally in tests of anxiety, locomotor activity, exploration of a novel environment, habituation to novelty and spatial learning. This phenotype is maintained on two different strain backgrounds, is rescued by transgenic expression of Thy-1 and by administration of the GABA, receptor antagonist pentylenetetrazole. Conclusions: The test for social transmission of food preference is based on the normal ability of mice in a colony to learn from each other which foods are safe to eat. The lack of this key survival behaviour in Thy-1 null mice could act as an evolutionary pressure point to conserve expression of Thy-1. Furthermore, the specific cognitive defect caused by inactivation of the Thy-1 gene suggests that it would be worthwhile to determine the role of Thy-1 in certain human familial forms of mental retardation that map to chromosome 11q22-23 in the region of the Thy-1 locus rather than the nearby ataxia telangiectasia locus. [References: 48]

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