Generation and Functional Analysis for GPI-anchored neural adhesion molecule NB-2 gene knockout mice.

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NB-2, a member of the contactin subgroup in the immunoglobulin superfamily, is restrictively expressed in the nervous system, reaching the maximum level at postnatal 3 weeks. NB-2 displays neurite outgrowth-promoting activity in vitro. To assess its function in the nervous system, we generated mutant mice ablating a part of NB-2 gene by replacing with the tau-LacZ gene. The general appearance of NB-2 deficient mice and the gross anatomical features were normal. The LacZ expression patterns in heterozygous mice revealed that NB-2 is preferentially expressed in the central auditory pathways. In the audiogenic seizure susceptibility (AGS) test, NB-2 mutant mice exhibited lower incidence of wild running, but higher rate of mortality than the wild-type littermates. c-Fos expression demonstrated that neural activity induced by the AGS in the NB-2 deficient mice was prominently attenuated in the both dorsal and external cortexes of inferior colliculus where enhanced neural activity is observed in the wild-type mice. Pure-tone stimulation after priming, NB-2 deficient mice exhibited a diffusive and low level of c-Fos expression in the central nucleus of inferior colliculus in comparison with a strong and a tonotopic banding expression of c-Fos in the wild-type littermates. Taken together, these results suggest that lack of NB-2 impairs the neuronal activity in the auditory system.