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Growth hormone-releasing hormone (GHRH), its receptor (GHRHR), and other members of the somatotropic axis are involved in non-rapid eye movement sleep (NREMS) regulation. Previously, studies established the involvement of hypothalamic GHRHergic mechanisms in NREMS regulation, but cerebral cortical GHRH mechanisms in sleep regulation remained uninvestigated. Here, we show that unilateral application of low doses of GHRH to the surface of the rat somatosensory cortex ipsilaterally decreased EEG delta wave power, while higher doses enhanced delta power. These actions of GHRH on EEG delta wave power occurred during NREMS but not during rapid eye movement sleep. Further, the cortical forms of GHRH and GHRHR were identical to those found in the hypothalamus and pituitary, respectively. Cortical GHRHR mRNA and protein levels did not vary across the day-night cycle, whereas cortical GHRH mRNA increased with sleep deprivation. These results suggest that cortical GHRH and GHRHR have a role in the regulation of localized EEG delta power that is state dependent, as well as in their more classic hypothalamic role in NREMS regulation. non-rapid eye movement sleep; somatotropic axis; sleep deprivation; slow-wave activity Address for reprint requests and other correspondence: J. M. Krueger, Washington State Univ., Coll. of Veterinary Medicine, Dept. of VCAPP, PO Box 646520, Pullman, WA 99164-6520 (e-mail: krueger@vetmed.wsu.edu )
AJP - Regulatory, Integrative and Comparative Physiology – The American Physiological Society
Published: Aug 1, 2007
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