A role for lipoprotein lipase during synaptic remodeling in the adult mouse brain

被引：39

作者：

Blain, JF

Paradis, E

Gaudreault, SB

Champagne, D

Richard, D

Poirier, J

机构：

[1] McGill Ctr Studies Aging, Verdun, PQ H4H 1R3, Canada

[2] McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ H4A 2B4, Canada

[3] Douglas Hosp, Res Ctr, Verdun, PQ H4H 1R3, Canada

[4] Univ Laval, Dept Anat & Physiol, Fac Med, St Foy, PQ G1K 7P4, Canada

来源：

NEUROBIOLOGY OF DISEASE | 2004年 / 15卷 / 03期

基金：

加拿大健康研究院;

关键词：

lipoprotein lipase; cholesterol; recycling; apolipoprotein E; entorhinal cortex lesion; hippocampus; degeneration; synaptic remodeling; proteoglycans;

D O I：

10.1016/j.nbd.2003.12.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Lipoprotein lipase (LPL) is a member of a lipase family known to hydrolyze triglyceride molecules found in lipoprotein particles. This particular lipase also has a role in the binding of lipoprotein particles to different cell-surface receptors. LPL has been identified in the brain but has no specific function yet. This study aimed at elucidating the role of LPL in the brain in response to injury. Mice were subjected to hippocampal deafferentation using the entorhinal cortex lesion and mRNA and protein expression were assessed over a time-course of degeneration/reinnervation. Hippocampal LPL levels peaked at 2 days post-lesion (DPL) both at the mRNA and protein levels. No change was observed for receptors of the LDL-receptor family or RAP at DPL 2 in the hippocampus but the glia-specific syndecan-4 was found to be significantly upregulated at DPL 2. These results suggest that LPL is involved in the recycling of cholesterol and lipids released from degenerating terminals after a lesion through a syndecan-4-dependent pathway. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：510 / 519

页数：10

共 60 条

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