Abstract
To date, the role of nitric oxide (NO) in mediation of cerebrovascular regulation during spreading depression (SD) in rats remains controversial. Studies are compromised by indirect assay of `regional' nitric oxide synthase activity (NOS) and/or inappropriate doses of antagonists. The present study utilises direct electrochemical detection in the pia to demonstrate a local, biphasic release of NO associated with each wave of cortical depolarisation. The mean peak of SD-induced NO release was 0.35 μM, which was significantly inhibited by l- N G-nitroarginine methyl ester ( l-NAME) pre-treatment. Changes in cerebrovascular flux remained intact following treatment with l-NAME, indicating little role for NO in mediation of rat SD blood-flux changes. Mean peak NO release was found to be lower than that observed in rat cerebral ischaemia studies (approximately 4 μM) and in SD in the cat gyrencephalic brain (approximately 0.8 μM).
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