Changes in Nitric Oxide Synthase and PKC activities in neonatal ionizing radiation cerebellum. Partial neuroprotec-tion by a treatment with 17-beta-estradiol

MARÍA AURELIA ZORRILLA ZUBILETE; DAFNE MAGALI SILBERMAN; LAURA RUTH GUELMAN; HUGO RÍOS; ANA MARÍA GENARO; LUIS MARÍA ZIEHER

Innsbruck

Congreso; 20th Biennial Meeting International Society for Neurochemistry (ISN), 21-26 August of 2005,; 2005

Increasing evidence has suggested that receptors for excitatory amino acids play an important role during cerebral ischemia. In this study we monitored the trafficking of NR2A/2B peptide, N-terminal domain of the N-methyl-D-aspartate receptor (NMDAR), from brain to blood after transient cerebral ischemia. The secondary endpoint of the study was the time course of NR2A/2B mRNA expression in brain and NR2A/2B antibodies development in blood of stroke animals. Adult male Sprague-Dawley rats were subjected to a transient focal ischemia induced by right middle cerebral artery occlusion. We found that the ischemia upregulated NR2A/2B mRNA with peak expression at 24 hour after reperfusion in cerebral cortex and at 0 hours in hippocampus. The level of NR2A/2B mRNA expression gradually declined from 2 to 72 hours in hippocampus. In contrast to the expression of mRNA, the level of  NR2A/2B protein, examined by Western blot, was reduced in the lesioned cortex and adjacent hippocampus at 0 and 24 hours. The extracellular trafficking of NR2 peptide due selective neuronal damage accompanied with decrease of the NMDAR distribution in the cortex at 0 h after reperfusion. In blood, the level of NR2A/2B peptide was significantly increased from 2 to 72 hours after stroke. In conclusion, our data suggest that cerebral ischemia induces early production of NR2A/2B peptide in bloodstream and may be used as a biomarker for acute brain ischemia.