Behavioral Alterations in Mice Lacking the Gene for Tenascin-X

Abstract

Tenascin-X (TNX) is the largest member in the tenascin family of large oligomeric glycoproteins of the extracellular matrix (ECM). TNX is expressed in the leptomeningeal trabecula and connective tissue of choroid plexus in the brain as well as in muscular tissues. Interestingly, single nucleotide polymorphism (SNP) analysis in human showed that TNX is significantly associated with schizophrenia. Previously we generated TNX-deficient (TNX−/−) mice by homologous recombination using embryonic stem (ES) cells. In the present study, we analyzed behaviors relevant to affect, learning and memory, and motor control in TNX−/− mice. TNX−/− mice showed increased anxiety in light–dark and open-field tests and superior memory retention in a passive avoidance test. Also, TNX−/− mice displayed higher sensorimotor coordination than did wild-type mice in a rotorod test. However, TNX−/− mice did not differ from wild-type mice in locomotor activity in a home-cage activity test using telemetric monitoring. These findings suggest that TNX has diverse roles including roles in behavioral functions such as anxiety, emotional learning and memory, and sensorimotor ability.