Abstract
Motor and cognitive phenotypes were assessed in mice deficient for the close homologue of the L1 adhesion molecule (CHL1). The CHL1-deficient mice displayed signs of decreased stress and a modification of exploratory behaviour. The mice also showed motor impairments on the Rotarod, but they were able to move as fast as controls in the alleys of a T-maze. The observed changes were assumed to be related to a deficit in attention. In addition, gender differences in CHL1 deficits were found and are discussed in view of a possible interaction with other cell adhesion molecules (CAMs) during development. The results are discussed in relation with motor and cognitive deficits in the human, caused by mutations of the distal part of the chromosome 3 which contains the CHL1 orthologue.