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Impaired motor coordination in mice lacking neural recognition molecule NB‐3 of the contactin/F3 subgroup

2003; Wiley; Volume: 56; Issue: 3 Linguagem: Inglês

10.1002/neu.10222

1097-4695

Yasuo Takeda, Keiko Akasaka, Sai Peck Lee, Satoru Kobayashi, Hitoshi Kawano, Shigeo Murayama, Naoki Takahashi, Kouichi Hashimoto, Masanobu Kano, Masahide Asano, Katsuko Sudo, Yoichiro Iwakura, Kazutada Watanabe,

Ion channel regulation and function

Abstract The neural recognition molecule NB‐3, which belongs to the contactin subgroup of the immunoglobulin superfamily, is expressed exclusively in the nervous system and mainly upregulated at the early postnatal stage during mouse brain development. The expression of NB‐3 in the cerebellum increases until adulthood. In contrast, the expression in the cerebrum declines to a low level after postnatal day 7. To characterize the functional roles of NB‐3 in vivo , we generated NB‐3‐deficient mice by substituting a part of the NB‐3 gene with the β‐galactosidase (Lac Z) gene. Complete overlap of the Lac Z expression in the heterozygous mouse brain with the NB‐3 immunostaining pattern in the rat cerebellum and with the previously reported pattern of in situ hybridization of NB‐3 transcripts indicated that Lac Z expression reflects the expression of NB‐3 in the mouse brain. NB‐3‐deficient mice were viable and fertile. The formation and organization of all nuclei and layers throughout the brains of mutant mice appeared normal. Behavioral tests to examine motor function showed that the mice deficient for NB‐3 were slow to learn to stay on the rotating rod in the rotorod test during repeated trials, and that they displayed dysfunction of equilibrium and vestibular senses in the wire hang and horizontal rod‐walking tests. In contrast, the mutant mice showed no difference of grasp force from the wild‐type mice. Thus, NB‐3‐deficient mice are impaired in motor coordination. © 2003 Wiley Periodicals, Inc. J Neurobiol 56: 252–265, 2003