Cortical spreading depression blocks the hyperthermic reaction induced by orexin a

• Published in: Neuroscience 2004, Vol.123 (2), p.567-574
• Main Authors: Monda, M, Viggiano, AN, Viggiano, AL, Fuccio, F, De Luca, V
• Format: Article
• Language: English
• Subjects: Adipose Tissue, Brown - innervation; Animals; Biological and medical sciences; body temperature; Carrier Proteins - administration & dosage; cerebral cortex; Cerebral Decortication; Cortical Spreading Depression; Fundamental and applied biological sciences. Psychology; Heart Rate - drug effects; Hyperthermia, Induced; Injections, Intraventricular; Intracellular Signaling Peptides and Proteins; Male; Neocortex - drug effects; Neocortex - physiology; Neuropeptides - administration & dosage; Orexins; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; rat; Rats; Rats, Sprague-Dawley; sympathetic activity; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology; thermogenesis; Thermogenesis - physiology; Vertebrates: nervous system and sense organs
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2003.09.016

This experiment tested the effect of cortical spreading depression on the sympathetic and thermogenic effects induced by orexin A. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures and heart rate were monitored in urethane-anesthetized male Sprague–Dawley rats before and 5 h after an injection of orexin A (1.5 nmol) into the lateral cerebral ventricle. The same variables were monitored in rats with cortical spreading depression, induced by an application of cotton pellets soaked with 2 M KCl to the frontal cortex. The results show that orexin A increases the sympathetic firing rate, IBAT and colonic temperatures and heart rate. The increases in firing rate, IBAT and colonic temperatures are blocked by cortical spreading depression, while the increase in heart rate is not affected by cortical spreading depression. These findings suggest that the cerebral cortex is involved in the control of the orexin A-induced hyperthermia. Furthermore, we suggested the name “hyperthermine A,” as additional denomination of “orexin A.”