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Brain serotonin depletion attenuates heatstroke-induced cerebral ischemia and cell death in rats

Brain serotonin depletion attenuates heatstroke-induced cerebral ischemia and cell death in rats AND METHODS BODY, Shydroxytryptamine (5HT; ) is located mainly in the gastrointestinal tract (8), blood platelets (9), central nervous system (5), and cerebral mast cells of certain species (22). When 5HT is applied directly to isolated cerebral vessels, a constriction occurs (7, 27), and this response can be inhibited by various concentrations of the 5-HT-receptor antagonists methysergide (7) and lysergic acid diethylamide (27). Furthe rmore, 5-HT has been postulated to be a candidate in the pathogenesis of a number of intracranial vascular diseases. For example, the release of 5-HT is said to occur after stroke (US), trauma (20), cold injury lesions (6), and cerebral ischemia (28). Our recent results show that cerebral ischemia is the main cause for neuronal damage during (11, 14, 15, 26). It is possible that 5-HT could be released from the central nervous system and thereby affect the -induced cerebral ischemia and neuronal damage. For these reasons, the effects of on cerebral ischemia and neuronal damage were determined in rats with normal brain 5-HT concentrations and in rats after brain 5-HT . IN THE Adult male Sprague-Dawley rats weighing 305 t 10 g were used. They were kept on a standard pellet diet and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Brain serotonin depletion attenuates heatstroke-induced cerebral ischemia and cell death in rats

Journal of Applied Physiology , Volume 80: 680 – Feb 1, 1996

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Publisher
The American Physiological Society
Copyright
Copyright © 1996 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
Publisher site
See Article on Publisher Site

Abstract

AND METHODS BODY, Shydroxytryptamine (5HT; ) is located mainly in the gastrointestinal tract (8), blood platelets (9), central nervous system (5), and cerebral mast cells of certain species (22). When 5HT is applied directly to isolated cerebral vessels, a constriction occurs (7, 27), and this response can be inhibited by various concentrations of the 5-HT-receptor antagonists methysergide (7) and lysergic acid diethylamide (27). Furthe rmore, 5-HT has been postulated to be a candidate in the pathogenesis of a number of intracranial vascular diseases. For example, the release of 5-HT is said to occur after stroke (US), trauma (20), cold injury lesions (6), and cerebral ischemia (28). Our recent results show that cerebral ischemia is the main cause for neuronal damage during (11, 14, 15, 26). It is possible that 5-HT could be released from the central nervous system and thereby affect the -induced cerebral ischemia and neuronal damage. For these reasons, the effects of on cerebral ischemia and neuronal damage were determined in rats with normal brain 5-HT concentrations and in rats after brain 5-HT . IN THE Adult male Sprague-Dawley rats weighing 305 t 10 g were used. They were kept on a standard pellet diet and

Journal

Journal of Applied PhysiologyThe American Physiological Society

Published: Feb 1, 1996

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