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.

Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity / Limatola, Cristina; Lauro, Clotilde; Catalano, Myriam; Ciotti, Mt; Bertollini, Cristina; DI ANGELANTONIO, Silvia; Ragozzino, Davide Antonio; Eusebi, Fabrizio. - In: JOURNAL OF NEUROIMMUNOLOGY. - ISSN 0165-5728. - STAMPA. - 166(1-2)(2005), pp. 19-28. [10.1016/j.jneuroim.2005.03.023]

Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity.

LIMATOLA, Cristina;LAURO, CLOTILDE;CATALANO, Myriam;BERTOLLINI, Cristina;DI ANGELANTONIO, SILVIA;RAGOZZINO, Davide Antonio;EUSEBI, Fabrizio
2005

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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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11573/364893
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