Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity

被引：128

作者：

Limatola, C

Lauro, C

Catalano, M

Ciotti, MT

Bertollini, C

Di Angelantonio, S

Ragozzino, D

Eusebi, F

机构：

[1] Univ Roma La Sapienza, Ctr Eccellenza BEMM, Ist Fisiol Umana & Farmacol, Dipartimento Fisiol Umana & Farmacol, I-00185 Rome, Italy

[2] Fdn Cenci Bolognetti, Ist Pasteur, I-00185 Rome, Italy

[3] Neuromed IRCCS, I-86077 Pozzilli, Italy

[4] CNR, Ist Neurobiol & Med Mol, I-00137 Rome, Italy

[5] Fdn Santa Lucia, I-00179 Rome, Italy

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2005年 / 166卷 / 1-2期

关键词：

glutamate; neuroprotection; fractalkine; ERK1/2; PI3K/Akt; AMPA current;

D O I：

10.1016/j.jneuroim.2005.03.023

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Excitotoxicity is a cell death caused by excessive exposure to glutamate (Glu), contributing to neuronal degeneration in many acute and chronic CNS diseases. We explored the role of fractalkin/CX(3)CL1 on survival of hippocampal neurons exposed to excitotoxic doses of Glu. We found that: CX(3)CL1 reduces excitotoxicity when co-applied with Glu, through the activation of the ERK1/2 and PI3K/Akt pathways, or administered up to 8 h after Glu insult; CX(3)CL1 reduces the Glu-activated whole-cell current through mechanisms dependent on intracellular Ca2+; CX(3)CL1 is released from hippocampal cells after excitotoxic insult, likely providing an endogenous protective mechanism against excitotoxic cell death. (C) 2005 Elsevier B.V. All rights reserved.

引用

页码：19 / 28

页数：10

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