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Mice lacking α1,3-fucosyltransferase IX demonstrate disappearance of Lewis x structure in brain and increased anxiety-like behaviors
Author(s) -
Takashi Kudo,
Takashi Fujii,
Shiro Ikegami,
Kaoru Inokuchi,
Yuko Takayama,
Yuzuru Ikehara,
Shoko Nishihara,
Akira Togayachi,
Takashi Sato,
Kouichi Tachibana,
Shinji Yuasa,
Hisashi Narimatsu
Publication year - 2006
Publication title -
glycobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.757
H-Index - 128
eISSN - 1460-2423
pISSN - 0959-6658
DOI - 10.1093/glycob/cwl047
Subject(s) - basolateral amygdala , glycolipid , neurite , forebrain , glycoprotein , neuroscience , microbiology and biotechnology , amygdala , biology , chemistry , medicine , central nervous system , biochemistry , in vitro
The 3-fucosyl-N-acetyllactosamine [Lewis x (Le(x)), CD15, SSEA-1] carbohydrate structure is expressed on several glycolipids, glycoproteins, and proteoglycans of the nervous system and has been implicated in cell-cell recognition, neurite outgrowth, and neuronal migration during development. To characterize the functional role of Le(x) carbohydrate structure in vivo, we have generated mutant mice that lack alpha1,3-fucosyltransferase IX (Fut9(-/-)). Fut9(-/-) mice were unable to synthesize the Le(x) structure carried on glycoproteins and glycolipids in embryonic and adult brain. However, no obvious pathological differences between wild-type and Fut9(-/-) mice were found in brain. In behavioral tests, Fut9(-/-) mice exhibited increased anxiety-like responses in dark-light preference and in elevated plus maze tests. Immunohistochemical analysis showed that the number of calbindin-positive neurons was decreased in the basolateral amygdala in Fut9(-/-) mice. These observations indicated that the carbohydrates synthesized by Fut9 play critical roles in functional regulations of interneurons in the amygdalar subdivisions and suggested a role for the Le(x) structure in some aspects of emotional behavior in mice.

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