| Summary: | 碩士 === 國防醫學院 === 生理學研究所 === 85 === Neurons release nitric oxide (NO) in response to activation of recptors for the excitatory amino acid N-methyl-D-aspartate (NMDA) . The goal of the present study was to examine whether NO is involved in the response of cerebral blood flow (CBF) to NMDA. Anesthetized male Sprague-Dawley rats were equipped with a cranial window. Regional CBF of the parietal cortex was monitored by laser-Doppler flowmetry. Topical application of NMDA (10-6 M and 10-5 M) for 5 minutes produced dose-dependent increases in CBF. Responses of CBF to NMDA were inhibited after the pretreatment with MK-801 (0.5 mg/kg iv) or tetrodotoxin (10-6 M; topical application) . MK-801 or tetrodotoxin, however, had no effect on acetylcholine (ACh; 10-7 M and 10-6 M)-induced increases in CBF. The selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole (7-NI; 50 mg/kg ip) also significantly inhibited the increases in CBF produced by NMDA, but not by ACh. In addition, responses of CBF to ACh, but not nitroglycerin, were inhibited by the nonspecific inhibitor of nitric oxide synthase NG-nitro-L-arginine (L-NNA, 10-4 M; topical application) . These findings suggest that increases in CBF produced by NMDA is mediated by neuronally derived NO and dependent on neuronal activation.
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