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)

Administration of 10 mg/kg TRH to mice was found to reduce the sleep and hypothermia induced by 4.7 g/kg ethanol. However, TRH did not reduce the sleep of mice that were given gamma-hydroxybutyric acid (GHBA), baclophen, or aminooxyacetic acid (AOAA) in combination with 3 g/kg/ ethanol. TRH also failed to reverse the hypothermia induced by the combination of ethanol and baclophen or GHBA, and the characteristic neurological effects of TRH e.g. tremor, increased muscle tone, and increased respiratory rate were reduced. In addition, TRH-induced locomotor stimulation was prevented by pretreatment with small doses of the GABA-ergic agents, and while 30 mg/kg TRH reduced the hypothermia produced by large doses of the GABA-ergic drugs, it did not antagonize the locomotor retardation produced by baclophen or GHBA. A hypothesis that the analeptic effects of TRH may be medicated via an inhibition of GABA systems is discussed.
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PMID:Antagonism of the analeptic activity of thyrotropin-releasing hormone (TRH) by agents which enhance GABA transmission. 1 50

The effects of gamma-hydroxybutyric acid (GHBA) on metabolic, respiratory and vasomotor activities and body temperature were assessed in unanesthetized rats at three different ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intraperitoneal administration of GHBA produced dose-dependent hypothermia in rats at both 8 and 22 degrees C Ta. At Ta = 8 degrees C the hypothermia was brought about solely by a decrease in metabolic heat production, while at Ta = 22 degrees C the hypothermia was due to both a decrease in metabolic heat production and an increase in cutaneous circulation (as indicated by changes in tail and foot skin temperatures). However, at Ta = 30 degrees C GHBA administration produced no changes in rectal temperature or other thermoregulatory parameters. Respiratory evaporative heat loss was not affected by GHBA application. Furthermore, it was found that the GHBA-induced hypothermia was antagonized by haloperidol (a selective blocker of dopamine receptors), but not by p-chlorophenylalanine (an inhibitor of serotonin synthesis). The data suggest that GHBA elicits a central dopamine receptor activation mainly via release of endogenous dopamine and leads to a hypothermia.
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PMID:Effects of gamma-hydroxybutyric acid on metabolic, respiratory and vasomotor activities and body temperature in rats. 15 42

The effect of nicotine on the neuroleptic-induced changes in striatal dopamine (DA) metabolism of mice was studied. To investigate the mechanism of action of nicotine, its interactions with apomorphine (APO) and gamma-hydroxybutyric acid (GHBA) were also investigated. Mice were given nicotine, (0.3-3 mg/kg subcutaneously) repeatedly (4 times) at 30 min. intervals. Haloperidol (HAL), (+/-)-sulpiride (SUL), APO or GHBA were administered after the second nicotine dose. Hexamethonium was given to prevent the effects of nicotine on autonomic ganglia. The striatal contents of DA and of its metabolites homovanillic acid (HVA), 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxytyramine (3-MT) were measured. The drug-induced hypothermia in mice was controlled by increasing ambient temperature. At ambient temperature of 32-34 degrees nicotine and HAL increased the striatal DOPAC and HVA contents additively, whereas APO counteracted the effects of nicotine at this ambient temperature. At 20-22 degrees nicotine decreased the 3-MT content which indicates reduced release of DA. In hypothermic mice nicotine inhibited better the HAL- and SUL-induced increases of HVA content than those of DOPAC content suggesting that the neuroleptic-induced increases in DOPAC and HVA contents are mediated partly by different mechanisms. In APO-treated mice both the GHBA- and nicotine-induced decreases of 3-MT content fell further. GHBA did not alter the nicotine-induced decrease of 3-MT content and so this effect of nicotine may be mediated indirectly via GABAergic neurones. Unlike GHBA and APO nicotine decreased 3-MT content only in hypothermic mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dual effects of nicotine on neuroleptic-induced changes of striatal dopamine metabolism in mice. 256 30

Administration of thyroliberin (TRH) to reserpinized mice causes tremor and counteracts the hypothermia in a dose-dependent fashion. The thyroliberin response is inhibited by gamma-hydroxybutyric acid (GHB) and baclofen, but not by other, more specific GABA-ergic agents, such as THIP, gamma-acetylenic GABA, and sodium valproate. Picrotoxin neither potentiates nor inhibits the thyroliberin actions. Nor are the thyroliberin effects dependent on cholinergic, monoaminergic or histaminergic mechanisms. The results repudiate a current hypothesis, that the peptide actions may be mediated by GABA-ergic pathways in the brain.
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PMID:Thermic and tremorogenic effects of thyroliberin (TRH) in reserpine-treated mice--the non-involvement of GABA-ergic mechanisms. 611 36

The endogenous brain constituent, gamma-hydroxybutyric acid (GHB), as well as its prodrug, gamma-butyrolactone (GBL), have recently gained interest in the drug addiction field due to their abuse potential and fatalities caused by overdose. It is known that GHB has two sites of actions: the gamma-aminobutyric acid(B) (GABA(B)) receptor and a specific-GHB binding site. The present study was designed to extend to GBL the investigations on the contribution of the GABA(B) receptor and the specific-GHB binding site to its in vivo effects. To this aim, DBA mice were pretreated either with GABA(B)-receptor antagonists, (3-aminopropyl)(diethoxymethyl)phosphinic acid (CGP 35348) and (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), or a putative antagonist of the specific-GHB binding site, 6,7,8,9-tetrahydro-5-hydroxy-5H-benzocyclohept-6-ylideneacetic acid (NCS-382), prior to the administration of doses of GBL that induced hypothermia, motor-incoordination (measured as motor-impairment at the Rota-Rod task), and sedation/hypnosis. The capability of SCH 50911 and NCS-382 to protect against GBL-induced lethality was also investigated. Pretreatment with either GABA(B)-receptor antagonist completely prevented GBL-induced hypothermia, motor-incoordination, and sedation /hypnosis. SCH 50911 also provided complete protection against GBL-associated lethality. Vice versa, NCS-382 failed to exert any antagonistic or protective effect. These results suggest that the in vivo GBL effects tested in the present study are mediated by activation of the GABA(B) receptor.
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PMID:Gamma-aminobutyric acidB (GABAB)-receptor mediation of different in vivo effects of gamma-butyrolactone. 1827 Apr 75