Release of hypothalamic corticotropin-releasing hormone and arginine-vasopressin by interleukin 1β and αMSH: studies in rats with different susceptibility to inflammatory disease

Żelazowski, Piotr; Patchev, Vladimir K.; Zelazowska, E; Chrousos, George P.; Gold, Philip W.; Sternberg, Esther M.

doi:10.1016/0006-8993(93)91181-q

Cited by 42 publications

(26 citation statements)

References 19 publications

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“…In contrast, both chronic NPY-induced obesity (55,56) and leptin deficiency (ob/ob and db/db mice) (57,58) result in profound hypercorticosteronemia in rodents. Acute central administration of ␣-MSH increased plasma ACTH and corticosterone (59,60), but our results suggest that the melanocortin system may not play an important role in the long-term control of the hypothalamopituitary adrenal (HPA) axis.…”

Section: Discussionmentioning

confidence: 55%

Effects of Chronic Central Nervous System Administration of Agouti-Related Protein in Pair-Fed Animals

Small

Kim²,

Stanley³

et al. 2001

Diabetes

145

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The melanocortin receptor (MC3-R and MC4-R) antagonist, agouti-related protein (AGRP), is a potent stimulant of food intake. We examined the effect of chronic intracerebroventricular (ICV) AGRP treatment on energy metabolism and pituitary function in ad libitum fed rats and rats administered AGRP and then pair-fed to a saline control group. Chronic ICV AGRP (83-132) administration (1 nmol/day for 7 days) significantly increased food intake and body weight in ad libitum fed animals compared with saline-treated controls (body weight on day 7: 272 ± 6 [saline] vs. 319 ± 8 g [AGRP ad libitum fed]; P < 0.001). A significant increase in the epididymal fat pad weight, interscapular brown adipose tissue (BAT) weight, and plasma leptin was also observed in the ad libitum fed group. In the AGRP pair-fed group, a significant increase in the epididymal fat pad weight, BAT weight, and plasma leptin was again observed, suggesting that AGRP caused metabolic changes independent of increased food intake. BAT uncoupling protein 1 (UCP-1) content was significantly decreased compared with saline controls in both the AGRP ad libitum fed (21 ± 8% of saline control; P < 0.01) and AGRP pair-fed groups (24 ± 7% of saline control; P < 0.01). Plasma thyroid-stimulating hormone (TSH) was significantly suppressed compared with saline controls in both the AGRP ad libitum fed and AGRP pair-fed groups (3. T he hypothalamic melanocortin system is a regulator of energy homeostasis. The agouti-related protein (AGRP), produced in the arcuate nucleus, is an antagonist at the melanocortin 3 and 4 receptors (MC3-R and MC4-R), which are distributed throughout the brain. The proopiomelanocortin (POMC) products, such as ␣-melanocyte-stimulating hormone (␣-MSH), act as agonists at the melanocortin receptors (1-3). Hypothalamic POMC mRNA, AGRP mRNA, and the density of MC4-R have been shown to be altered with nutritional status (4,5). Defects of POMC processing and mutations of MC4-R in humans and mice are associated with gross obesity (6-11).5Administration of the synthetic MC3/4-R agonist MT II into the forebrain ventricles or directly into the paraventricular nucleus (PVN) of the hypothalamus of rats or mice produced a dosage-dependent reduction in food intake and body weight (12)(13)(14). A single injection of either the endogenous (AGRP ) or the synthetic (SHU9119 and HS014) MC3/4-R antagonists stimulated food intake in rodents (12,13,15,16). Chronic administration of the more selective MC4-R antagonist, HS028, for 7 days via an osmotic minipump significantly increased food intake and body weight. Tachyphylaxis to HS028 did not occur. However, neither energy expenditure nor pituitary function were examined in this study (17). Previous results from this department have demonstrated that AGRP (83-132), the endogenous hypothalamic melanocortin receptor antagonist, significantly increased 24-h food intake and antagonized the anorectic effects of ␣-MSH (16).The melanocortin system also influences energy expenditure. Intracerebroventricular (ICV) administra...

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Section: Discussionmentioning

confidence: 55%

Effects of Chronic Central Nervous System Administration of Agouti-Related Protein in Pair-Fed Animals

Small

Kim²,

Stanley³

et al. 2001

Diabetes

145

View full text Add to dashboard Cite

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“…As such, differences between these two strains in IL-1-induced alterations in central CRH and/or HPA axis activity do not dramatically alter the duration of the SWS enhancement after IL-1. This is not the case for Fischer 344 rats, in which the duration of SWS enhancement after this dose of IL-1 lasts for almost 5 h. This result was not expected because the HPA axis response of Fischer 344 rats to IL-1 is greater than in Lewis or Sprague-Dawley rats [this study, 5, 16]which we thought would result in a shorter duration of SWS enhancement due to subsequent inhibition of IL-1 actions in the CNS by corticosterone. Additional experiments are necessary to determine the central mechanisms responsible for the prolonged increase in duration of IL-1-induced SWS in this rat strain.…”

Section: Discussionmentioning

confidence: 72%

“…The time course and magnitude of IL-1-induced alterations in sleep-wake behavior differ between Sprague-Dawley, Fischer 344, and Lewis rat strains in a manner consistent with the hypothesis that CRH is both a modulator of responses to IL-1 and involved in the regulation/modulation of waking. The role of CRH in modulating responses to IL-1 is further demonstrated by the finding that pretreatment with the CRH receptor antagonist α-hCRH attenuates the initial increase in waking observed in Fischer 344 rats, a strain that demonstrates increased CRH release in response to IL-1 [4, 16]. …”

Section: Discussionmentioning

confidence: 99%

“…For example, central or systemic administration of CRH into rats, rabbits, and humans increases waking [12, 19, 20, 21], whereas blockade of CRH receptors reduces waking [14, 22]. Fischer 344 rats produce more CRH in response to IL-1 than do Lewis rats [4, 16]which is in turn reflected in circulating adrenocorticotropic hormone and/or corticosterone [e.g., 5]; this study]. The findings that sleep is almost entirely absent during the 2nd postinjection hour after IL-1 and that IL-1-induced corticosterone concentrations at this time point are greater in Fischer 344 rats than in the other strains suggest that IL-1-induced CRH is one mediator of this response.…”

Section: Discussionmentioning

confidence: 99%

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Rat Strains that Differ in Corticotropin-Releasing Hormone Production Exhibit Different Sleep-Wake Responses to Interleukin 1

Opp

Imeri

2001

Neuroendocrinology

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Corticotropin-releasing hormone (CRH) is a mediator of responses to a variety of stressors, including immune challenge. CRH and the hypothalamic-pituitary-adrenal (HPA) axis constitute a negative feedback mechanism for actions of immunomodulators, such as interleukin (IL) 1. CRH is a potent inducer of waking, whereas IL-1 induces slow-wave sleep (SWS). We hypothesize that the complex changes in sleep-wake behavior during immune challenge are mediated in part by CRH and its antagonism of IL-1-induced enhancement of SWS. To further explore this hypothesis, we administered IL-1β intracerebroventricularly into rats of genetically related strains that differ in CRH/HPA axis responsiveness to IL-1 and determined subsequent alterations in their sleep-wake behavior. Sprague-Dawley rats responded to central administration of IL-1 with alterations in sleep-wake behavior as previously reported; SWS increased, and rapid eye movement sleep (REMS) and waking decreased. CRH and the HPA axis of Lewis rats are reported to be hyporesponsive to challenge; the onset of the IL-1-induced increase in SWS was quicker and the peak magnitude of the response greater than in Sprague-Dawley rats. In contrast, Fischer 344 rats exhibit greater CRH release and HPA axis activation in response to IL-1. IL-1 induced a profound and transient increase in waking of Fischer 344 rats before SWS increased. The febrile responses to IL-1 of Fischer 344 and Lewis rats were identical and of greater magnitude than those observed in Sprague-Dawley rats. Pretreatment with the CRH receptor antagonist α-helical CRH_(9–41) blocked the initial IL-1-induced increase in waking of Fischer 344 rats. CRH receptor blockade did not affect the IL-1-induced alterations in sleep-wake behavior of Lewis or Sprague-Dawley rats or brain temperature of any rat strain. These observations support the hypothesis that CRH is both a modulator of responses to IL-1 and is involved in the regulation of waking.

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“…Various other abnormalities in neural pathways known to both regulate these neuroendocrine responses and to modulate inflammation are seen in Lewis rats, including blunted late-phase, sympathoneuronal noradrenergic responses to glucoprivic stress (27). Lewis rats also exhibit enhanced IL-1-induced hypothalamic secretion of arginine vasopressin (AVP) compared with Fischer rats (28), suggesting a shift in Lewis rats from CRH to AVP control of the stress response. Such shifts from a primarily CRH to AVP driven stress response have been shown to occur in situations of chronic stress, such as chronic peripheral inflammation and after a single injection of IL-1 (29).…”

mentioning

confidence: 99%

Neural-immune interactions in health and disease.

Sternberg¹

1997

J. Clin. Invest.

325

163

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Release of hypothalamic corticotropin-releasing hormone and arginine-vasopressin by interleukin 1β and αMSH: studies in rats with different susceptibility to inflammatory disease

Cited by 42 publications

References 19 publications

Effects of Chronic Central Nervous System Administration of Agouti-Related Protein in Pair-Fed Animals

Effects of Chronic Central Nervous System Administration of Agouti-Related Protein in Pair-Fed Animals

Rat Strains that Differ in Corticotropin-Releasing Hormone Production Exhibit Different Sleep-Wake Responses to Interleukin 1

Neural-immune interactions in health and disease.

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