Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sauvagine is a 40 amino acid peptide, isolated from the skin of the South American frog, Phyllomedusa sauvagei, and structurally related to mammalian corticotropin releasing factor (CRF). Experiments with centrally or peripherally injected sauvagine produced dose-dependent hypothermia in rats kept at ambient temperatures of +4 degrees C and +22 degrees C, but no effect was seen on rats maintained at +34 degrees C. To determine whether a pituitary-adrenal dependent step was involved, the thermoregulatory response was studied in hypophysectomized, adrenalectomized and sham-operated rats maintained at a room temperature of +22 degrees C. Significant hypothermia was produced in all three experimental groups, showing that this response is not mediate by the pituitary-adrenal axis. CRF had no effect on the thermoregulatory functions of rats and furthermore alpha-helical CRF (9-41), a CRF receptor antagonist, which inhibited the pituitary and cardiovascular actions of sauvagine, did not modify the thermoregulatory response in rats.
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PMID:Sauvagine: effects on thermoregulation in the rat. 233 Mar 43

Corticotropin-releasing factor (CRF) has been shown to reverse effect of pentobarbital (PbNa) within the central nervous system. In this study, the mechanism of the antagonistic effect of CRF on PbNa-induced anesthesia and hypothermia in rats was examined. Intraventricular administration of CRF significantly shortened sleeping time and antagonized hypothermia induced by PbNa. Propranolol (148 micrograms, 0.5 mumol), a beta-blocker, completely reversed the CRF effect, although propranolol alone affected neither sleeping time nor rectal temperature. Phentolamine, an alpha-blocker, reversed the antagonistic effect of CRF on PbNa, though the same dose of phentolamine alone increased the sleeping time in the absence of CRF. Atropine, an anticholinergic agent, did not affect the ability of CRF to reverse the effects of PbNa. These results suggest that the ability of CRF to reduce some of the effects of PbNa may be mediated at least in part by brain beta-noradrenergic receptors.
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PMID:Corticotropin-releasing factor reverses the effect of pentobarbital through a beta-noradrenergic mechanism in rats. 284 61

To investigate the mechanism by which ACTH secretion is inhibited during hypothermia, hypophysial portal blood was collected from euthermic and hypothermic rats, and the concentrations of corticotropin-releasing factor (CRF), vasopressin (AVP), and oxytocin (OT) were measured by RIA. Whereas CRF levels in portal plasma were not different in the two groups, AVP and OT levels were significantly lower in hypothermic rats. The concentration of AVP and OT in peripheral plasma was also significantly lower in hypothermic rats compared with euthermic controls. The pituitary responsiveness to CRF during hypothermia was tested in vivo and in vitro. In pentobarbital-anesthetized male rats injected iv with 0.1 or 1.0 nmol CRF, the ACTH response was significantly smaller in hypothermic compared with euthermic animals. However, hemipituitaries superfused at 31 C released the same amount of ACTH in response to 1 nM CRF as hemipituitaries superfused at 37 C (31 C, 541 +/- 90 pg; 37 C, 563 +/- 29 pg) despite reduced baseline secretion (31 C, 77 +/- 10 pg/10 min; 37 C, 114 +/- 14 pg/10 min; P less than 0.05). The data suggest that the inhibition of ACTH secretion during hypothermia is mediated by decreased hypothalamic secretion of AVP and OT which in turn decreases the pituitary responsiveness to CRF.
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PMID:Inhibition of corticotropin release during hypothermia: the role of corticotropin-releasing factor, vasopressin, and oxytocin. 298 77

The effects of corticotropin-releasing factor (CRF) on pentobarbital-induced sleeping time and hypothermia in rats were studied. Intraventricular administration of CRF significantly shortened the sleeping time induced by pentobarbital injection (50 mg/kg b.wt.) in a dose-dependent manner. CRF also attenuated the hypothermic effect of pentobarbital. However, peripheral administration of CRF did not affect the action of pentobarbital. alpha-Helical CRF9-41, CRF antagonist, reversed the effects of CRF. These results suggest that CRF antagonizes the effects of pentobarbital within the central nervous system.
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PMID:The antagonistic effect of corticotropin-releasing factor on pentobarbital in rats. 349 Feb 96

Corticotropin-releasing hormone (CRH) overproduction and serotonergic dysfunction have both been implicated in a range of psychiatric disorders, such as anxiety and depression, and several studies have shown interactions between these two neurotransmitter systems. In this study, we investigated the effects of CRH challenge on hypothalamo-pituitary-adrenal (HPA) axis activity in female transgenic mice overproducing CRH. Furthermore, the effects of mild stress on HPA axis activity and body temperature were investigated in these mice. Pre- and post-synaptic 5-HT1A receptor function were studied by monitoring body temperature and plasma corticosterone levels after challenge with the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propyl-amino)-tetralin (8-OH-DPAT). Hypothermia in response to 8-OH-DPAT treatment did not differ between transgenic and wild type mice, indicating unaltered somatodendritic 5-HT1A autoreceptor function in mice overproducing CRH. In wild type mice 8-OH-DPAT increased plasma corticosterone levels, but not in transgenic animals. CRH injection, however, increased corticosterone levels in both groups. These data suggest desensitization of post-synaptic, but not pre-synaptic, 5-HT1A receptors in mice overproducing CRH. These findings resemble those seen in depressed patients following 5-HT1A challenge, which is in accord with the hypothesized role of CRH in the pathogenesis of depression.
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PMID:Mice overexpressing CRH show reduced responsiveness in plasma corticosterone after a5-HT1A receptor challenge. 1288 73

Prevailing changes in the feeding status or the nutritional status, in general, can modify the expression of many orexigenic and anorexigenic peptides, which influence hypothalamic functions. These peptides usually adjust body temperature according to anabolic (increased appetite with suppressed metabolic rate and body temperature) or catabolic (anorexia with enhanced metabolism and temperature) patterns. It was plausible to presume that such peptides contribute to regulated changes of body temperature (either fever or hypothermia) in systemic inflammation, particularly since anorexia is a common feature in inflammatory processes. No consistent, common, or uniform way of action was, however, demonstrated, which could have described the effects of various peptides. With the exception of cholecystokinin (CCK), all investigated peptides were devoid of real thermoregulatory actions: they influenced the metabolic rate (and consequently body temperature), but not the mechanisms of heat loss. Central CCK is indeed catabolic and may participate in febrigenesis. Leptin may activate various cytokines, catabolic peptides and may inhibit anabolic peptides, but it probably has no direct febrigenic effect and it is not indispensable in fever. Melanocortins and corticotropin-releasing factor provide catabolic adaptive mechanisms to food intake (diet induced thermogenesis) and environmental stress, respectively, but they act rather as endogenous antipyretic substances during systemic inflammation, possibly contributing to the mechanisms of limitation of fever. Bacterial lipopolysaccharides enhance the expression of most of these catabolic peptides. In contrast, neuropeptide Y (NPY) expression may not be changed, only its release is decreased at specific nuclei, a defective NPY effect may also contribute to the febrile rise in body temperature. The data provide no clear-cut explanation for the mechanism of hypothermia seen in systemic inflammation. According to speculations, a presumed, overflow,-type release of NPY from the hypothalamic nuclei, as well as a suppression of the activity of catabolic peptides, could possibly cause hypothermia. There are no cues, however, referring to the identity of factors that could trigger such changes during systemic inflammation in order to induce hypothermia.
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PMID:Orexigenic vs. anorexigenic peptides and feeding status in the modulation of fever and hypothermia. 1535 11

The urocortin1 (Ucn1) neurons of the mid-brain-localized Edinger-Westphal nucleus (EW) are robustly responsive to ethanol (EtOH) administration, and send projections to the dorsal raphe nucleus (DRN), which contains corticotropin-releasing factor type 2 receptors (CRF2) that are responsive to Ucn1. In addition, the DRN has been shown to be involved in regulation of body temperature, a function greatly affected by EtOH administration. The goal of the present study was to identify the role that the urocortinergic projections from the EW to the DRN have in mediating EtOH-induced and lipopolysaccharide (LPS)-induced hypothermia. Male C57BL6/J mice were used. Groups of mice underwent cannulation of the DRN, and then received i.p. injections of EtOH (2g/kg) or LPS (600 microg/kg or 400 microg/kg), followed by intra-DRN injections of artificial cerebrospinal fluid (aCSF) or anti-sauvagine (aSVG) (55 pmol), a CRF2 antagonist. Separate groups of mice received single intra-DRN injections of Ucn1 (20 pmol), CRF (20 pmol) or aCSF. For all experiments, core temperatures were monitored rectally every 30 min for several hours post-injection. Both EtOH and LPS induced hypothermia, and aSVG significantly attenuated this effect after EtOH; however, there was no significant attenuation of hypothermia after either dose of LPS. Ucn1 injection also caused hypothermia, while CRF injection did not. These data demonstrate that EtOH-induced hypothermia, but not LPS-induced hypothermia, may involve Ucn1 from EW acting at CRF2 receptors in the DRN.
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PMID:Ethanol versus lipopolysaccharide-induced hypothermia: involvement of urocortin. 1596 90

O,O,S-Trimethylphosphorothioate (OOS-TMP), an impurity present in various organophosphorus insecticides, has previously been shown to induce hypophagia. The major goal of this study was to investigate its mechanism of action. Both intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) injection transiently induced hypophagia at a dose of 5mg/kg within 6h, without causing lung injury. Hypophagia was accompanied by up-regulation of corticotropin releasing factor (CRF) (2.92+/-0.45 vs. 1.7+/-0.5, at 2h after i.c.v., 3.40+/-1.38 vs. 1.76+/-0.41 at 6h after i.p., P<0.05) in the hypothalamus. After i.c.v. injection, hypophagia recovered by 6h after dosing. At doses higher than 5mg/kg, i.c.v. injection induced continuous hypophagia from 20min to 72h after dosing, accompanied by hypothermia and lung injury. OOS-TMP was considered to induce hypophagia through enhancing expression of CRF.
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PMID:Roles of neuropeptides in O,O,S-trimethylphosphorothioate (OOS-TMP)-induced anorexia in mice. 1769 39

To determine the mechanism of sensitivity to low-temperature exposure (20 degrees C for 3h) and corticotropin-releasing factor (CRF) induced increased homeothermy, we investigated gene transcripts of putative thermogenic proteins and mitochondrial fatty acid (FA)-oxidation enzymes in neonatal chicks. The hypothalamic-pituitary-adrenal (HPA) axis in low-temperature-exposed neonatal chicks was activated by central administration of CRF. Neonatal chicks showed hypothermia on exposure to low-temperature, with no enhancement of HPA axis and gene transcripts of avian adenine nucleotide translocator, avian uncoupling protein, avian peroxisome-proliferator-activated receptor-gamma co-activator-1alpha, and mitochondrial FA transport and oxidation enzymes in vital organs. However, central administration of CRF activated the HPA axis under low environmental temperature and induced increased homeothermy that was associated with the enhancement of gene transcripts and activities of mitochondrial FA-oxidation enzymes in the liver and heart.
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PMID:Homeothermy in neonatal chicks exposed to low environmental temperature with or without intracerebroventricular administration of corticotropin-releasing factor. 1869 76

Energy balance of the body is determined mainly by the function of various hypothalamic and brainstem nuclei, according to a complex interaction between the regulation of body temperature (actual metabolic rate vs. heat loss) and regulation of body weight (metabolic rate vs. food intake). The direct effect of central anabolic neuropeptides (neuropeptide Y, orexins, melanin concentrating hormone, etc.) is to enhance food intake and suppress metabolic rate with a tendency to cause hypothermia, while central catabolic neuropeptides (melanocortins, corticotropin releasing factor, cocaine-amphetamine regulated peptide, etc.) suppress food intake and enhance energy expenditure with a tendency to induce hyperthermia. Many other neuropeptides are neither clearly anabolic, nor clearly catabolic, but still influence these complex hypothalamic/brainstem functions. Some peripheral peptides (e.g. leptin, insulin, ghrelin) acting at either peripheral or cerebral sites also contribute to the regulation of energy balance. The prevailing thermoregulatory status, the substances or neural signals representing actual feeding vs. established nutritional states, and the aging process may modify the expression and/or activity of peripheral and central peptides and peptide receptors.
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PMID:Thermoregulation, energy balance, regulatory peptides: recent developments. 2051 39


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