Effect of restraint stress on food intake and body weight is determined by time of day.

Three experiments were conducted to investigate the effect of restraint stress applied at different times of the light-dark cycle on feeding behavior and body weight of rats. Sprague-Dawley rats were restrained for 3 h in restraining tubes either at the start or the end of the light cycle. There was a significant reduction in food intake on the day of restraint and no change in food intake during a 10-day recovery period in either experiment. Reductions of food intake on the day of restraint were about the same for both restrained groups compared with their controls. When stress was applied in the evening, eating was inhibited during the first 2 h after restraint, whereas in rats restrained in the morning, feeding was suppressed twice: during the 4 h after restraint and during the first 2 h of the dark cycle. Restraint induced a significant weight loss that was greater in the rats stressed in the morning. Neuropeptide Y (NPY) levels determined at the time of food suppression for both experiments (beginning of the dark cycle) revealed an elevation of NPY in the paraventricular nucleus of rats stressed in the morning compared with other groups, but no difference in hypothalamic NPY mRNA expression. Expression of uncoupling protein mRNA in brown adipose tissue and leptin mRNA in epididymal fat, measured at the start of the dark period, was not altered by stress. There was an elevation of dopamine turnover in the hypothalami of rats restrained at the end of light cycle, but not those restrained in the morning. These results show that restraint stress has a greater effect on metabolism and energy balance when it is applied in the morning. Additional studies are needed to elucidate mechanisms involved in the suppression of food intake 9 h after restraint.

[1]  D. Richard,et al.  Role of CRH in the effects of 5-HT-receptor agonists on food intake and metabolic rate. , 1996, The American journal of physiology.

[2]  G. Koob,et al.  Appetite-Suppressing Effects of Urocortin, a CRF-Related Neuropeptide , 1996, Science.

[3]  L. Campfield,et al.  Feeding inhibition by neuropeptide Y , 1996, Nature.

[4]  R. Harris,et al.  Early and late stimulation of ob mRNA expression in meal-fed and overfed rats. , 1996, The Journal of clinical investigation.

[5]  M. Smith,et al.  Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic paraventricular nucleus during repeated stress: association with reduction in glucocorticoid receptor mRNA levels. , 1995, Endocrinology.

[6]  M. Schwartz,et al.  Effect of Intracerebroventricular Insulin Infusion on Diabetic Hyperphagia and Hypothalamic Neuropeptide Gene Expression , 1995, Diabetes.

[7]  P. J. Larsen,et al.  Chronic Administration of Glucocorticoids Directly Upregulates Prepro‐Neuropeptide Y and Y1‐Receptor mRNA Levels in the Arcuate Nucleus of the Rat , 1994, Journal of neuroendocrinology.

[8]  B. Jeanrenaud,et al.  Hypothalamic Neuropeptide Y Messenger Ribonucleic Acid Levels in Pre‐Obese and Genetically Obese (fa/fa) Rats; Potential Regulation Thereof by Corticotropin‐Releasing Factor , 1993, Journal of neuroendocrinology.

[9]  H. McCarthy,et al.  Increased neuropeptide Y concentrations in specific hypothalamic nuclei of the rat following treatment with methysergide: Evidence that NPY may mediate serotonin's effects on food intake , 1993, Peptides.

[10]  G. Koob,et al.  Corticotropin-releasing factor in the paraventricular nucleus modulates feeding induced by neuropeptide Y , 1993, Brain Research.

[11]  Y. Oomura,et al.  In vivo measurement of hypothalamic serotonin release by intracerebral microdialysis: Significant enhancement by immobilization stress in rats , 1992, Brain Research Bulletin.

[12]  C. Nemeroff,et al.  Physiology and pharmacology of corticotropin-releasing factor. , 1991, Pharmacological reviews.

[13]  N. Rothwell,et al.  Involvement of corticotrophin releasing factor (CRF) in the thermogenic and anorexic actions of serotonin (5-HT) and related compounds , 1991, Brain Research.

[14]  M. Dallman,et al.  Stress-induced adrenocorticotropin secretion: diurnal responses and decreases during stress in the evening are not dependent on corticosterone. , 1991, Endocrinology.

[15]  G. Bray,et al.  Effect of corticotropin releasing hormone and neuropeptide Y on electrophysiological activity of sympathetic nerves to interscapular brown adipose tissue , 1990, Neuroscience.

[16]  C. Nemeroff,et al.  Effects of 5-HT1A receptor agonists on hypothalamo-pituitary-adrenal axis activity and corticotropin-releasing factor containing neurons in the rat brain. , 1990, European journal of pharmacology.

[17]  M. Herkenham,et al.  Altered expression of hypothalamic neuropeptide mRNAs in food-restricted and food-deprived rats. , 1990, Neuroendocrinology.

[18]  D. Krahn,et al.  The anorectic effects of CRH and restraint stress decrease with repeated exposures , 1990, Biological Psychiatry.

[19]  Y. Oomura,et al.  Stress-induced anorexia in rats mediated by serotonergic mechanisms in the hypothalamus , 1989, Physiology & Behavior.

[20]  J. Morley,et al.  Behavioral effects of corticotropin-releasing factor: localization and characterization of central effects , 1988, Brain Research.

[21]  S. Kalra,et al.  Food deprivation and ingestion induce reciprocal changes in neuropeptide Y concentrations in the paraventricular nucleus , 1988, Peptides.

[22]  G. Kennett,et al.  5-HT1B agonists induce anorexia at a postsynaptic site. , 1987, European journal of pharmacology.

[23]  S. Leibowitz,et al.  Neuropeptide Y chronically injected into the hypothalamus: A powerful neurochemical inducer of hyperphagia and obesity , 1986, Peptides.

[24]  G. Kennett,et al.  Female rats are more vulnerable than males in an animal model of depression: the possible role of serotonin , 1986, Brain Research.

[25]  D. Krahn,et al.  CRF antagonist partially reverses CRF- and stress-induced effects on feeding , 1986, Brain Research Bulletin.

[26]  G. Koob,et al.  Corticotropin releasing factor produces behavioural activation in rats , 1982, Nature.

[27]  E. Stricker,et al.  Effects of dopamine-depleting brain lesions on experimental hyperphagia in rats , 1982, Physiology & Behavior.

[28]  M. Palkovits,et al.  Isolated removal of hypothalamic or other brain nuclei of the rat. , 1973, Brain research.

[29]  V. Critchlow,et al.  Effects of Diurnal Variation in Plasma Corticosterone Levels on Adrenocortical Response to Stress.∗ , 1967, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[30]  N. Ling,et al.  Involvement of corticotropin-releasing factor in restraint stress-induced anorexia and reversion of the anorexia by somatostatin in the rat. , 1988, Life sciences.