α-Ketoisocaproic acid regulates phosphorylation of intermediate filaments in postnatal rat cortical slices through ionotropic glutamatergic receptors

被引：27

作者：

Funchal, C ^{[1
]}

Pelaez, PD ^{[1
]}

Loureiro, SO ^{[1
]}

Vivian, L ^{[1
]}

Pessutto, FDB ^{[1
]}

de Almeida, LMV ^{[1
]}

Wofchuk, ST ^{[1
]}

Wajner, M ^{[1
]}

Pureur, RP ^{[1
]}

机构：

[1] Univ Fed Rio Grande do Sul, Inst Ciencias Basicas Saude, Dept Bioquim, BR-90035003 Porto Alegre, RS, Brazil

来源：

DEVELOPMENTAL BRAIN RESEARCH | 2002年 / 139卷 / 02期

关键词：

maple syrup urine disease; cytoskeleton; development; phosphorylation; glutamatergic receptor;

D O I：

10.1016/S0165-3806(02)00578-3

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

In this study we investigated the effects of a-ketoisocaproic acid (KIC), the main keto acid accumulating in the inherited neurometabolic disorder maple syrup urine disease (MSUD), on the in vitro incorporation of P-32 into intermediate filament (IF) proteins from cerebral cortex of rats during development. KIC decreased the in vitro incorporation of P-32 into the IF proteins studied up to day 12, had no effect on day 15, and increased this phosphorylation in cortical slices of 17- and 21-day-old rats. A similar effect on IF phosphorylation was achieved along development by incubating cortical slices with glutamate. Furthermore, the altered phosphorylation caused by the presence of KIC in the incubation medium was mediated by the ionotropic receptors NMDA, AMPA and kainate up to day 12 and by NMDA and AMPA in tissue slices from 17- and 21-day-old rats. The results suggest that alterations of IF phosphorylation may be associated with the neuropathology of MSUD. (C) 2002 Published by Elsevier Science B.V.

引用

页码：267 / 276

页数：10

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