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Neuropharmacology. 2013 Apr;67:267-71. doi: 10.1016/j.neuropharm.2012.11.023. Epub 2012 Dec 3.

Immunotherapy blocking the tissue plasminogen activator-dependent activation of N-methyl-D-aspartate glutamate receptors improves hemorrhagic stroke outcome.

Author information

1
Inserm UMR-S U919, Serine Proteases and Pathophysiology of the Neurovascular Unit, GIP Cyceron, University Caen Lower-Normandy, Boulevard Becquerel, Caen, France. thomas.gaberel@hotmail.fr

Abstract

Ischemic and hemorrhagic strokes have different etiologies, but share some pathogenic mechanisms, including a pro-neurotoxic effect of endogenous tissue plasminogen activator (tPA) via N-methyl-d-Aspartate (NMDA) receptors. Thus, in a model of intracerebral hemorrhage in rats, we investigated the therapeutic value of a strategy of immunotherapy (αATD-GluN1 antibody) preventing the interaction of tPA with NMDA receptors. We found that a single intravenous injection of αATD-GluN1 reduced brain edema, neuronal death, microglial activation and functional deficits following intracerebral hemorrhage, without affecting the hematoma volume.

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