Title |
Fractalkine/CX3CL1 engages different neuroprotective responses upon selective glutamate receptor overactivation
|
---|---|
Published in |
Frontiers in Cellular Neuroscience, January 2015
|
DOI | 10.3389/fncel.2014.00472 |
Pubmed ID | |
Authors |
Clotilde Lauro, Myriam Catalano, Eleonora Di Paolo, Giuseppina Chece, Ida de Costanzo, Flavia Trettel, Cristina Limatola |
Abstract |
Neuronal death induced by overactivation of N-methyl-d-aspartate receptors (NMDARs) is implicated in the pathophysiology of many neurodegenerative diseases such as stroke, epilepsy and traumatic brain injury. This toxic effect is mainly mediated by NR2B-containing extrasynaptic NMDARs, while NR2A-containing synaptic NMDARs contribute to cell survival, suggesting the possibility of therapeutic approaches targeting specific receptor subunits. We report that fractalkine/CX3CL1 protects hippocampal neurons from NMDA-induced cell death with a mechanism requiring the adenosine receptors type 2A (A2AR). This is different from CX3CL1-induced protection from glutamate (Glu)-induced cell death, that fully depends on A1R and requires in part A3R. We show that CX3CL1 neuroprotection against NMDA excitotoxicity involves D-serine, a co-agonist of NR2A/NMDAR, resulting in cyclic AMP-dependent transcription factor cyclic-AMP response element-binding protein (CREB) phosphorylation. |
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Other | 4 | 8% |
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