Endocrinology, Vol 122, 1343-1348, Copyright © 1988 by Endocrine Society

ARTICLES

Circadian variations in plasma corticosterone permit normal termination of adrenocorticotropin responses to stress

L Jacobson, SF Akana, CS Cascio, J Shinsako and MF Dallman
Department of Physiology, University of California School of Medicine, San Francisco 94143.

We previously reported that adrenalectomized rats given constant corticosterone via a sc pellet (B-PELLET) hypersecrete ACTH in response to stress. Although lacking a feedback signal, B-PELLET rats do not secrete ACTH indefinitely after stress; plasma ACTH levels in these animals returned to those in sham-operated (SHAM) rats within 1-4 h after 2-min restraint. To distinguish between the requirement for circadian or stress-induced increases in corticosterone, we compared changes in ACTH and corticosterone levels after stress in SHAM and B- PELLET rats with those in cyanoketone-treated rats (CK) and adrenalectomized rats given corticosterone in their drinking fluid (B- WATER). B-WATER rats exhibited sustained increases in plasma corticosterone after lights-off, correlating with the nocturnal feeding period. Morning plasma corticosterone levels in B-WATER rats were constant and even lower than those in B-PELLET rats; however, B-WATER rats did not differ from SHAM rats in their ACTH response to ip injection. CK rats, which have an approximately normal circadian corticosterone rhythm but do not have significant corticosterone responses to acute stimuli, also exhibited plasma ACTH levels similar to those of SHAM rats at all times after 5-min restraint. Compared with SHAM and B-WATER rats in the same experiment, B-PELLET rats tended to hypersecrete ACTH 60 min after 5 min of restraint, but only had significantly elevated plasma ACTH relative to both groups 45 min after 10 min of restraint. We conclude that circadian, rather than stress- induced, increases in corticosterone may be sufficient for normal termination of ACTH responses to stress.

This article has been cited by other articles:

				A. D. Mueller, M. S. Pollock, S. E. Lieblich, J. R. Epp, L. A. M. Galea, and R. E. Mistlberger Sleep deprivation can inhibit adult hippocampal neurogenesis independent of adrenal stress hormones Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1693 - R1703. [Abstract] [Full Text] [PDF]

				M. Girotti, M. S. Weinberg, and R. L. Spencer Differential Responses of Hypothalamus-Pituitary-Adrenal Axis Immediate Early Genes to Corticosterone and Circadian Drive Endocrinology, May 1, 2007; 148(5): 2542 - 2552. [Abstract] [Full Text] [PDF]

				A. Jaferi and S. Bhatnagar Corticosterone Can Act at the Posterior Paraventricular Thalamus to Inhibit Hypothalamic-Pituitary-Adrenal Activity in Animals that Habituate to Repeated Stress Endocrinology, October 1, 2006; 147(10): 4917 - 4930. [Abstract] [Full Text] [PDF]

				P. Gip, G. Hagiwara, R. M. Sapolsky, V. H. Cao, H. C. Heller, and N. F. Ruby Glucocorticoids influence brain glycogen levels during sleep deprivation Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2004; 286(6): R1057 - R1062. [Abstract] [Full Text] [PDF]

				M. Fleshner, T. Deak, K. T. Nguyen, L. R. Watkins, and S. F. Maier Endogenous Glucocorticoids Play a Positive Regulatory Role in the Anti-Keyhole Limpet Hemocyanin In Vivo Antibody Response J. Immunol., March 15, 2001; 166(6): 3813 - 3819. [Abstract] [Full Text] [PDF]

				F. S. Dhabhar and B. S. McEwen Enhancing versus suppressive effects of stress hormones on skin immune function PNAS, February 2, 1999; 96(3): 1059 - 1064. [Abstract] [Full Text] [PDF]

				B. Nock, T. J. Cicero, and M. Wich Chronic Exposure to Morphine Decreases Physiologically Active Corticosterone in Both Male and Female Rats but by Different Mechanisms J. Pharmacol. Exp. Ther., August 1, 1998; 286(2): 875 - 882. [Abstract] [Full Text]

				B. K. Taylor, S. F. Akana, M. A. Peterson, M. F. Dallman, and A. I. Basbaum Pituitary-Adrenocortical Responses to Persistent Noxious Stimuli in the Awake Rat: Endogenous Corticosterone Does Not Reduce Nociception in the Formalin Test Endocrinology, May 1, 1998; 139(5): 2407 - 2413. [Abstract] [Full Text] [PDF]

				S. M. Nair, T. R. Werkman, J. Craig, R. Finnell, M. Joels, and J. H. Eberwine Corticosteroid Regulation of Ion Channel Conductances and mRNA Levels in Individual Hippocampal CA1 Neurons J. Neurosci., April 1, 1998; 18(7): 2685 - 2696. [Abstract] [Full Text] [PDF]

				K. T. Nguyen, T. Deak, S. M. Owens, T. Kohno, M. Fleshner, L. R. Watkins, and S. F. Maier Exposure to Acute Stress Induces Brain Interleukin-1beta Protein in the Rat J. Neurosci., March 15, 1998; 18(6): 2239 - 2246. [Abstract] [Full Text] [PDF]

				T. Deak, J. L. Meriwether, M. Fleshner, R. L. Spencer, A. Abouhamze, L. L. Moldawer, R. E. Grahn, L. R. Watkins, and S. F. Maier Evidence that brief stress may induce the acute phase response in rats Am J Physiol Regulatory Integrative Comp Physiol, December 1, 1997; 273(6): R1998 - R2004. [Abstract] [Full Text] [PDF]

				B. Nock, M. Wich, and T. J. Cicero Chronic Exposure to Morphine Increases Corticosteroid-Binding Globulin J. Pharmacol. Exp. Ther., September 1, 1997; 282(3): 1262 - 1268. [Abstract] [Full Text]

				S. F. Akana and M. F. Dallman Chronic Cold in Adrenalectomized, Corticosterone (B)-Treated Rats: Facilitated Corticotropin Responses to Acute Restraint Emerge as B Increases Endocrinology, August 1, 1997; 138(8): 3249 - 3258. [Abstract] [Full Text] [PDF]