Arginine-nitric oxide pathway and cerebrovascular regulation in cortical spreading depression

Arginine-nitric oxide pathway and cerebrovascular regulation in cortical spreading depression MATERIALS AND METHODS SPREADING (CSD)is ashort-lasting depolarization wave that moves across the cerebral cortex at a rate of 2-5 mm/min. A brief phase of excitation is immediately followed by prolonged nerve cell , which is synchronous with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, and enhanced energy metabolism (6,13,22,23). CSD is accompanied by major changes of cerebral blood flow (CBF) (12, 22, 23), and CSD is used as an animal model for migraine (22, 23). N-methyl-D-aspartate (NMDA)-receptor activation is essential for the propagation of CSD (23), constituting a transmembrane pathway for Ca2+ influx, the proper stimulus for constitutive NO synthase (NOS) activity in endothelial cells and in nervous tissue (8, 24). The guanosine 3’,5’-cyclic monophosphate (cGMP) content in the cortex increases by 200-400% for several minutes (lo), and extracellular L-arginine decreases transiently during CSD (6), suggesting NO production. This raised CORTICAL 0363-6135/95 $3.00 Copyright o 1995 Animal preparation. Fifty-eight male Wistar rats (300-350 g) were anesthetized with halothane (Vapor, Drager; 4% induction, 1.5% during surgery and 0.7% maintenance) in O2 30%-N20 70%. Catheters were inserted in a femoral artery and a femoral vein, and the trachea was cannulated. After relaxation http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Arginine-nitric oxide pathway and cerebrovascular regulation in cortical spreading depression

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Publisher
The American Physiological Society
Copyright
Copyright © 1995 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

MATERIALS AND METHODS SPREADING (CSD)is ashort-lasting depolarization wave that moves across the cerebral cortex at a rate of 2-5 mm/min. A brief phase of excitation is immediately followed by prolonged nerve cell , which is synchronous with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, and enhanced energy metabolism (6,13,22,23). CSD is accompanied by major changes of cerebral blood flow (CBF) (12, 22, 23), and CSD is used as an animal model for migraine (22, 23). N-methyl-D-aspartate (NMDA)-receptor activation is essential for the propagation of CSD (23), constituting a transmembrane pathway for Ca2+ influx, the proper stimulus for constitutive NO synthase (NOS) activity in endothelial cells and in nervous tissue (8, 24). The guanosine 3’,5’-cyclic monophosphate (cGMP) content in the cortex increases by 200-400% for several minutes (lo), and extracellular L-arginine decreases transiently during CSD (6), suggesting NO production. This raised CORTICAL 0363-6135/95 $3.00 Copyright o 1995 Animal preparation. Fifty-eight male Wistar rats (300-350 g) were anesthetized with halothane (Vapor, Drager; 4% induction, 1.5% during surgery and 0.7% maintenance) in O2 30%-N20 70%. Catheters were inserted in a femoral artery and a femoral vein, and the trachea was cannulated. After relaxation

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Jul 1, 1995

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