Biomedical subjects

L C Payne

Publications and source records attributed to L C Payne.

12 recordsLinked to original sources

PubMed1995

Growth-hormone-releasing hormone mediates the sleep-promoting activity of interleukin-1 in rats.

The involvement of endogenous growth-hormone-releasing hormone (GHRH) in the sleep-promoting activity of interleukin-1 (IL1) was studied. The effects on sleep of intracerebroventricular injection of IL1 were tested in rats pretreated with intracerebroventricular antibodies to GHRH (GHRH-ab). One group of rats received two treatments each consisting of two injections, control IgG + physiological saline (IgG + Sal) and on another day GHRH-ab + Sal, whereas another group of rats received IgG + Sal, IgG + IL1 and GHRH-ab + IL1 on separate days with one day off between the various treatments. IgG or GHRH-ab was injected 6 h prior to dark onset; Sal or IL1 was administered at dark onset. Recording of sleep-wake activity and cortical brain temperature (Tcrt) was started with the injection of IgG or GHRH-ab and continued for 18 h. GHRH-ab (GHRH-ab + Sal) suppressed rapid eye movement sleep (REMS), non-REMS (NREMS) and EEG slow-wave activity (SWA) during NREMS throughout the recording period. IL1 treatment (IgG + IL1) enhanced NREMS and SWA, and induced fever for 6 h. Pretreatment with GHRH-ab (GHRH-ab + IL1) abolished the IL1-induced increases in NREMS, attenuated the enhancements in SWA, and suppressed fever for 6 hours after IL1. The results indicate that the sleep-promoting activity of IL1 is mediated at least in part via GHRH. The suppression of the IL1-induced fever by GHRH-ab might be attributed to an inhibition of hypothalamic somatostatin.

Animals↗

PubMed1994

Induction of pituitary sensitivity to interleukin-1: a new function for corticotropin-releasing hormone.

Activation of the hypothalamic-pituitary-adrenal axis to release corticotropin-releasing hormone (CRH), corticotropin (ACTH), and glucocorticoids during inflammatory stress is now considered a key function of interleukin-1 (IL-1). Current dogma suggests that in vivo ACTH release due to IL-1 is indirect and entirely results from IL-1-mediated-CRH release from the hypothalamus. The present findings show that low levels of exogenous or endogenous CRH can sensitize the pituitary gland to the direct ACTH releasing activity of IL-1. Once sensitized, IL-1 induced ACTH release is not inhibitable by the CRH antagonist, alpha-helical (alpha h) CRF [9-41]. Thus, IL-1 effects ACTH release at the level of both the hypothalamus and pituitary gland. Perhaps more importantly, the results suggest pituitary sensitization to cytokines, such as IL-1, as a new function for CRH. This action would represent a novel interactive point between the nervous, endocrine, and immune systems whereby very mild psychological or physical stress could have a profound impact on an inflammatory response by increasing pituitary sensitivity to immunological mediators such as IL-1.

Adrenocorticotropic Hormone↗

PubMed1994

Effects of streptozotocin-induced diabetes on lymphocyte POMC and growth hormone gene expression in the rat.

Diabetes in the rat is associated with a change in the profiles of several neuroendocrine hormones resulting in poor growth and decreased immune function. Since lymphocytes can also serve as a source of neuroendocrine hormones, we have examined whether the change in hormone profiles are accompanied by an impairment of lymphocyte GH and POMC gene expression in the immune system. Diabetes was induced by the administration of streptozotocin (STZ; 10 mg/100 g body weight) and 3 days later GH and ACTH protein and mRNA were determined. The results show a modest diminution of GH RNA in the spleen of diabetic animals whereas the expression of POMC mRNA and ACTH by the thymus was enhanced. The expression of POMC in the spleen appeared unaltered while the increase of POMC RNA in the thymus was evident after the first day of STZ treatment. STZ had no direct effect on GH or POMC expression in the spleen or thymus cells in vitro. Insulin does not appear to be involved in the expression of lymphocyte GH or POMC. The administration of insulin to the diabetic animals had no significant effect on the expression of GH or POMC by the immune cells. In addition, lymphocytes do not appear to serve as a source of insulin or are the expression of genes for lymphocyte GH or ACTH altered by insulin in vitro. Taken together, the findings are the first to report on the expression of neuroendocrine genes in lymphocytes during diabetes. The mechanism for the inhibition of GH and stimulation of POMC expression by lymphocytes in diabetic animals is unknown, but it is tempting to speculate an important role in the development of the autoimmunity that characterizes this complex disease.

Adrenocorticotropic Hormone↗

PubMed1993

Hypothalamic releasing hormones mediating the effects of interleukin-1 on sleep.

There is a substantial literature describing the interactions between the endocrine and immune systems. Although such interactions are less well known within the brain, one major brain function altered during inflammation and infection and by several endocrine hormones is sleep. Pathological disturbances, be they inflammation, infectious disease, and/or sleep deprivation, result in altered hypothalamus-pituitary function and cytokine metabolism. In respect to hormone secretion from the pituitary, cytokines are now recognized to play an important role in modulating the neuroendocrine system. Changes in sleep provide a useful illustration of the interactions between cytokines and the hypothalamus-pituitary axis. Evidence linking interleukin-1 (IL-1) to growth hormone releasing hormone and to corticotropin releasing hormone in regard to their effects on sleep is reviewed.

Animals↗

PubMed1992

Interactions of cytokines with the hypothalamus-pituitary axis.

Major humoral mechanisms include the endocrine and immune systems, and there is substantial literature describing interactions between these systems during infection and inflammatory processes. Within the brain, such interactions are less well known. One major brain function altered during infection and inflammation and by several endocrine hormones is sleep. These changes in sleep provide a useful illustration of the interactions between cytokines and the hypothalamus-pituitary axis (HPA). Experimental evidence is reviewed that illustrates the interaction of cytokines, especially interleukin-1 (IL-1), with the HPA in regard to their effect on sleep. The evidence linking IL-1, growth hormone-releasing hormone/growth hormone, and corticotropin-releasing hormone to sleep regulation is reviewed. There is also evidence that shows that these two major sleep-regulatory systems are linked to each other.

Cytokines↗

PubMed1992

Stimulation and inhibition of growth hormone secretion by interleukin-1 beta: the involvement of growth hormone-releasing hormone.

The effects of intracerebroventricularly (i.c.v.) injected interleukin-1 beta (IL-1 beta: 1, 2.5, 10, and 25 ng) were studied on plasma growth hormone (GH) and prolactin (PRL) concentrations in freely moving rats chronically implanted with i.c.v. cannulas and intracardial catheters. Significant changes in PRL secretion were not found. Small i.c.v. doses of IL-1 stimulated GH secretion 15 min postinjection (significant after 2.5 ng IL-1) whereas high doses of IL-1 suppressed plasma GH concentrations. The stimulation of GH secretion by 2.5 ng IL-1 was abolished when endogenous growth hormone-releasing hormone (GHRH) was immunoneutralized by pretreating the rats with GHRH antibodies. The results indicate that IL-1 elicits GH secretion by stimulating the release of hypothalamic GHRH. The inhibition of GH secretion after high doses of IL-1 is attributed to the previously reported corticotropin-releasing-hormone-releasing activity of IL-1.

Animals↗

PubMed1991

Cholecystokinin promotes sleep and reduces food intake in diabetic rats.

It has been reported that systemic injections of cholecystokinin (CCK) elicit the behavioral characteristics of satiety, including sleep, in rats. CCK is a potent stimulator of insulin secretion, and insulin is hypothesized to be involved in sleep and feeding regulation. The purpose of the current experiments was to study the possible role of endogenous insulin in the food-intake-reducing and hypnogenic effects of intraperitoneally (IP) administered CCK. Normal and streptozotocin (STR)-diabetic rats were injected with isotonic saline or CCK (10 and 50 micrograms/kg) at dark onset, and sleep-wake activity was determined for the next 12 h. There were no significant differences between the baseline sleep-wake activity of normal and diabetic rats. IP injection of CCK elicited a selective increase in nonrapid-eye-movement sleep in both groups during the first postinjection hour. In a separate experiment, the effects of CCK (10 micrograms/kg) on food intake were determined in control and diabetic rats; CCK suppressed the 1-h food intake in both groups. In a third experiment, the effects of CCK treatment (50 micrograms/kg) on plasma insulin levels were determined. In normal rats, CCK elicited a two-fold increase in plasma insulin concentration, whereas diabetic rats had a significantly lower basal insulin level which was not affected by CCK treatment. We conclude that hypnogenic and food-intake-reducing effects of exogenously administered CCK are closely associated; however, pancreatic insulin does not play a significant role in either of these effects.

Animals↗

PubMed1968