http://www.cnr.it/ontology/cnr/individuo/prodotto/ID4610
Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity. (Articolo in rivista)
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- Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity. (Articolo in rivista) (literal)
- Anno
- 2005-01-01T00:00:00+01:00 (literal)
- Alternative label
Limatola C.1, Lauro C.2, Catalano M.3, Ciotti M.T.4, Bertollini C.5, Di Angelantonio S.6, Ragozzino D.7, Eusebi F.8 (2005)
Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity.
in Journal of neuroimmunology (Print)
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- Limatola C.1, Lauro C.2, Catalano M.3, Ciotti M.T.4, Bertollini C.5, Di Angelantonio S.6, Ragozzino D.7, Eusebi F.8 (literal)
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- ISI Web of Science (WOS) (literal)
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- 1,2,3,5,6,7,8 = Istituto Pasteur-Fondazione Cenci Bolognetti and Dipartimento di Fisiologia Umana e Farmacologia, Centro di Eccellenza BEMM, Università di Roma La Sapienza, P.le A. Moro 5, 00185 Rome, Italy;
1,6,7 = Neuromed I.R.C.C.S., Via Atinese 18, I86077 Pozzilli, Italy;
4 =Istituto di Neurobiologia e Medicina Molecolare, CNR, Viale Marx 43, 00137 Rome, Italy;
8 = Fondazione Santa Lucia, via Ardeatina 306, 00179 Rome, Italy.
(literal)
- Titolo
- Chemokine CX3CL1 protects rat hippocampal neurons against glutamate-mediated excitotoxicity. (literal)
- 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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