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

Citation
V. Mayeux-portas et al., Mice lacking the cell adhesion molecule Thy-1 fail to use socially transmitted cues to direct their choice of food, CURR BIOL, 10(2), 2000, pp. 68-75
Citations number
48
Categorie Soggetti
Experimental Biology
Journal title
CURRENT BIOLOGY
ISSN journal
09609822 → ACNP
Volume
10
Issue
2
Year of publication
2000
Pages
68 - 75
Database
ISI
SICI code
0960-9822(20000127)10:2<68:MLTCAM>2.0.ZU;2-C
Abstract
Background: Thy-1 is a major cell-surface glycoprotein of mature neurons an d certain other cells, including those of the lymphoreticular system. Despi te being the simplest member of the immunoglobulin superfamily, the biologi cal 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 neurol ogical or behavioural effects being apparent. Results: We show here that Thy-1 null mice are unable to make the appropria te dietary choice in the test for social transmission of food preference, d espite showing a normal level of social interaction with the demonstrator m ouse, normal neophobia, and normal learning in a T-maze using scented food as cues. The mice also performed normally in tests of anxiety, locomotor ac tivity, exploration of a novel environment, habituation to novelty and spat ial learning. This phenotype is maintained on two different strain backgrou nds, 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 o n the normal ability of mice in a colony to learn from each other which foo ds are safe to eat. The lack of this key survival behaviour in Thy-1 null m ice could act as an evolutionary pressure point to conserve expression of T hy-1. Furthermore, the specific cognitive defect caused by inactivation of the Thy-1 gene suggests that it would be worthwhile to determine the role o f Thy-1 in certain human familial forms of mental retardation that map to c hromosome 11q22-23 in the region of the Thy-1 locus rather than the nearby ataxia telangiectasia locus.