Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity

Cristina Limatola, Clotilde Lauro, Myriam Catalano, Maria Teresa Ciotti, Cristina Bertollini, Silvia Di Angelantonio, Davide Ragozzino, Fabrizio Eusebi

Research output: Contribution to journalArticlepeer-review


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: CX 3CL1 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.

Original languageEnglish
Pages (from-to)19-28
Number of pages10
JournalJournal of Neuroimmunology
Issue number1-2
Publication statusPublished - Sep 2005


  • AMPA current
  • ERK1/2
  • Fractalkine
  • Glutamate
  • Neuroprotection
  • PI3K/Akt

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology


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