Mice lacking α1,3-fucosyltransferase IX demonstrate disappearance of Lewis x structure in brain and increased anxiety-like behaviors

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Abstract
The 3-fucosyl-N-acetyllactosamine [Lewis x (Lex), 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 Lex carbohydrate structure in vivo, we have generated mutant mice that lack α1,3-fucosyltransferase IX (Fut9−/−). Fut9−/− mice were unable to synthesize the Lex 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 Lex structure in some aspects of emotional behavior in mice.

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