Nitric oxide does not mediate cerebral blood flow changes during cortical spreading depression in the anaesthetised rat

Nitric oxide does not mediate cerebral blood flow changes during cortical spreading depression in... 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 μ M, 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 μ M) and in SD in the cat gyrencephalic brain (approximately 0.8 μ M). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neuroscience Letters Elsevier

Nitric oxide does not mediate cerebral blood flow changes during cortical spreading depression in the anaesthetised rat

Neuroscience Letters, Volume 250 (2) – Jun 19, 1998

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Publisher
Elsevier
Copyright
Copyright © 1998 Elsevier Science Ireland Ltd
ISSN
0304-3940
D.O.I.
10.1016/S0304-3940(98)00442-X
Publisher site
See Article on Publisher Site

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 μ M, 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 μ M) and in SD in the cat gyrencephalic brain (approximately 0.8 μ M).

Journal

Neuroscience LettersElsevier

Published: Jun 19, 1998

References

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