Nitric oxide of neuronal origin mediates NMDA-induced cerebral hyperemia in rats.
The goal of this study was to determine whether neuronally derived nitric oxide mediates responses of cerebral blood flow (CBF) to N-methyl-D-aspartate (NMDA). In anesthetized Sprague-Dawley rats, regional CBF of the parietal cortex was monitored by laser-Doppler flowmetry. Topical application of either NMDA or acetylcholine produced concentration-related increases in CBF. Responses of CBF to NMDA (10(-5) M) but not to acetylcholine were inhibited (0+/-3% vs 21+/-5%, p < 0.05) by 7-nitroindazole (50 mg/kg, i.p.). MK-801 (0.5 mg/kg, i.v.) and tetrodotoxin (10(-6) M, topical application) also inhibited NMDA-induced responses. These results suggest that nitric oxide of neuronal origin mediates NMDA-induced increases in CBF.
PubMed Abstracts
PubMed Abstracts