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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.