Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9194560 | Journal of Neuroimmunology | 2005 | 10 Pages |
Abstract
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 fractalkine/CX3CL1 on survival of hippocampal neurons exposed to excitotoxic doses of Glu. We found that: CX3CL1 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; CX3CL1 reduces the Glu-activated whole-cell current through mechanisms dependent on intracellular Ca2+; CX3CL1 is released from hippocampal cells after excitotoxic insult, likely providing an endogenous protective mechanism against excitotoxic cell death.
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Authors
Cristina Limatola, Clotilde Lauro, Myriam Catalano, Maria Teresa Ciotti, Cristina Bertollini, Silvia Di Angelantonio, Davide Ragozzino, Fabrizio Eusebi,