Nitric oxide does not mediate cerebral blood flow changes during cortical spreading depression in the anaesthetised rat.
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 microM, 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 microM) and in SD in the cat gyrencephalic brain (approximately 0.8 microM).
Neuroscience Research, SmithKline Beecham Pharmaceuticals, New Frontiers Science Park, Essex, UK.
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D000758:Anesthesia; D000818:Animals; D002540:Cerebral Cortex / Q000098:blood supply*; D013181:Cortical Spreading Depression / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D009569:Nitric Oxide