Corticotropin-releasing hormone in the lateral parabrachial nucleus inhibits sodium appetite in rats

1 Department of Physiology, Health Sciences Institute, Federal University of Bahia, Bahia, Brazil; and 2 Departments of Psychology and Pharmacology, and the Cardiovascular Center, University of Iowa, Iowa City, Iowa Submitted 7 February 2003 ; accepted in final form 8 December 2005 The present study investigated the role of corticotropin-releasing hormone (CRH) in the lateral parabrachial nucleus (LPBN) in the behavioral control of body fluid homeostasis by determining the effect of bilateral injections of the CRH receptor antagonist, -helical corticotropin-releasing factor (CRF) 9–41 , and the CRH receptor agonist, CRH, on sodium chloride (salt appetite) and water (thirst) intake. Groups of adult, male Sprague-Dawley rats had stainless-steel cannulas implanted bilaterally into the LPBN and were sodium depleted or water deprived. Bilateral injections of -helical CRF 9–41 into the LPBN significantly potentiated water and salt intake in the sodium-depleted rats when access to fluids was restored. Bilateral injections of -helical CRF 9–41 into the LPBN (1.0 µg) also increased sodium appetite in water-deprived rats. Conversely, in sodium-depleted animals, bilateral injections of CRH inhibited sodium chloride intake. These results suggest that there is an endogenous CRH inhibitory mechanism operating in the LPBN to modulate the intake of sodium (salt appetite). This mechanism may contribute to the behavioral control of restoration of body fluid homeostasis in sodium-deficient states. water intake; -helical corticotropin-releasing factor Address for reprint requests and other correspondence: A. K. Johnson, Dept. of Psychology, Univ. of Iowa, Iowa City, IA 52242–1407 (E-mail: alan-johnson{at}uiowa.edu )