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2014 Fiscal Year Final Research Report

Functional analysis of alpha1,6-fucosyltransferase deficient mice and underlying molecular mechanism

Research Project

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Project/Area Number 24590087
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Biological pharmacy
Research InstitutionTohoku Pharmaceutical University

Principal Investigator

FUKUDA Tomohiko  東北薬科大学, 薬学部, 准教授 (40433510)

Project Period (FY) 2012-04-01 – 2015-03-31
Keywords糖転移酵素 / フコース / 膜タンパク質 / AMPA 受容体
Outline of Final Research Achievements

We previously reported thatα1,6-fucosyltransferase (Fut8) knockout (Fut8-/-) mice showed a schizophrenia-like phenotype and a decrease in working memory. To understand the underlying molecular mechanism, we analyzed early-form long-term potentiation (E-LTP), which is closely related to learning and memory in the hippocampus. The scale of E-LTP induced by high frequency stimulation was significantly decreased in Fut8-/- mice. The expression levels of AMPARs in the postsynaptic density were enhanced in Fut8-/- mice, although there were no significant differences in the total expression levels, implicating that AMPARs without core fucosylation might exist in an active state. Taken together, loss of core fucosylation on AMPARs enhanced their heteromerization, which might increase sensitivity for postsynaptic depolarization, and persistently activate N-methyl-D-aspartate receptors as well as Ca2+ influx and CaMKII, and then impair LTP.

Free Research Field

糖鎖生物学

URL: 

Published: 2016-06-03  

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