title: Aberrant responses to acoustic stimuli in mice deficient for neural recognition molecule NB-2.
abstract: NB-2, a member of the contactin subgroup in the immunoglobulin superfamily, is expressed specifically in the postnatal nervous system, reaching a maximum level at 3 weeks postnatal. NB-2 displays neurite outgrowth-promoting activity in vitro. To assess its function in the nervous system, we generated mutant mice in which a part of the NB-2 gene was ablated and replaced with the tau-LacZ gene. The general appearance of NB-2-deficient mice and their 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 test, NB-2-deficient mice exhibited a lower incidence of wild running, but a higher mortality rate than the wild-type littermates. c-Fos immunohistochemistry demonstrated that neural excitability induced by the audiogenic seizure test in the NB-2-deficient mice was prominently attenuated in both the dorsal and external cortices of the inferior colliculus, where enhanced neural excitability was observed in the wild-type mice. In response to pure-tone stimulation after priming, NB-2-deficient mice exhibited a diffuse and low level of c-Fos expression in the central nucleus of the inferior colliculus, which was distinctly different from the band-like c-Fos expression corresponding to the tonotopic map in the wild-type littermates. Taken together, these results suggest that a lack of NB-2 causes impairment of the neuronal activity in the auditory system.
authors.affiliation: Department of Cell Recognition, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173-0015, Japan.
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Takeda
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Niki
authors.forename: Junko
authors.initials: J
authors.lastname: Ogawa
authors.forename: Satoru
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kai
authors.forename: Keiko
authors.initials: K
authors.lastname: Akasaka
authors.forename: Masahide
authors.initials: M
authors.lastname: Asano
authors.forename: Katsuko
authors.initials: K
authors.lastname: Sudo
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
authors.forename: Kazutada
authors.initials: K
authors.lastname: Watanabe
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D001306:Auditory Pathways / Q000378:metabolism / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism; D015816:Cell Adhesion Molecules, Neuronal / Q000172:deficiency* / Q000235:genetics; D058966:Contactins; D017930:Genes, Reporter; D016762:Genes, fos / Q000502:physiology; D007150:Immunohistochemistry; D007763:Lac Operon / Q000235:genetics; D051379:Mice; D008817:Mice, Mutant Strains; D012640:Seizures / Q000235:genetics / Q000503:physiopathology*
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; C104187:Cntn5 protein, rat; D058966:Contactins