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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

Cessation of chronic ethanol administration, and elimination of ethanol from the body, results in a withdrawal syndrome in mice characterized by behavioural symptoms and hypothermia. During withdrawal, the accumulation rate of [14C] 5-hydroxytryptamine (5-HT) from [14C]tryptophan, was significantly lower in the brainstem of the ethanol-withdrawn animals than in controls. A similar pattern was seen in forebrain. When the rate of 5-HT accumulation was determined using pargyline, no differences occurred between control and ethanol-treated animals. The endogenous concentrations of tryptophan in plasma, and tryptophan, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in brain were the same in ethanol-treated and control animals. It is suggested that the changes in accumulation of 14C-5-HT and 14C-5-HIAA in ethanol-withdrawn animals reflected alterations in electrical activity of serotoninergic neurons during withdrawal.
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PMID:Neurochemical correlates of ethanol withdrawal: alterations in serotoninergic function. 1 95

The tranquillising activity of 3-[gamma-(p-fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazino [1, 2-a]quinoline hydrochloride (centpyraquin), a new adrenergic neurone blocking antihypertensive agent, has been evaluated in various laboratory animals. The compound has a calming effect in mice, rats, cats and monkeys. In low doses it reduces the spontaneous motor activity followed in progressively higher doses by hypothermia, ptosis and catalepsy and a taming effect in monkeys and cats. It potentiates pentobarbitone-, hexobarbitone- and ethanol-induced sleep and antagonises amphetamine induced toxicity in mice. It, however, fails to antagonise morphine induced mania and hyperactivity in cats. It blocks conditioned avoidance response in rats at a much lower dose (ED50 = 2.73 mg/kg) than the unconditioned response (ED50 = 10,9 mg/kg). In cats centpyraquin increases the voltage and slows the frequency of cortical EEG discharges. Centpyraquin has the profile of activity of a neuroleptic on the central nervous system.
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PMID:Pharmacological studies on 3-[gamma-(p-fluorobenzoyl)propyl]-2,3,4,4a,5,6-hexahydro-1-(H)-pyrazino ]1,2-a] quinoline hydrochloride (compound 69/183). Part III: Assessment of tranquillising activity. 3 55

Rats were rendered tolerant to ethanol by daily gavage of 4--5 g/kg. The degree of motor impairment on the moving belt test and of hypothermia after i.p. test doses of ethanol was measured prior to and at various times during the chronic treatment, to assess the rates of tolerance development. L-Tryptophan (75 mg/kg twice daily) was administered chronically to elevate brain serotonin level. This treatment did not alter the motor impairment or hypothermia produced by the initial test doses of ethanol (2.0 and 2.5 g/kg respectively). However, the development of tolerance to both the motor impairment and hypothermia effects of ethanol was accelerated in the tryptophan-treated rats. This finding complements our earlier observations that depletion of 5-HT with p-CPA slows down tolerance. Blood ethanol measurements at 20 min (motor impairment) or 90 min (hypothermia) after the administration of the test dose reveal no significant difference between the control and tryptophan-treated rats, suggesting that tryptophan did not influence the metabolism of ethanol. This finding supports the hypothesis that brain serotonin modulates the development of tolerance to ethanol.
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PMID:Effect of L-tryptophan on the acquisition of tolerance to ethanol-induced motor impairment and hypothermia. 10 29

Acquisition and retention of a shock avoidance task were impaired in mice at 5 h and 5 days but not at 14 days after withdrawal from 5 days of chronic alcohol consumption. Mice trained before ingestion of an alcohol-containing diet showed impairment in retention of the shock avoidance procedure 5 h after withdrawal from the diet but not during ingestion or 5 days after withdrawal. At 5 h after withdrawal from the alcohol-containing diet, motor activity and sensitivity to shock were not affected, but there was a decreased motor response to shock. There was no correlation between performance of the avoidance task and the severity of withdrawal signs, as measured by hypothermia or convulsions on handling. The hypothermia and other withdrawal signs were reversed by acute injection of alcohol, but the impairment in avoidance responding was not. These results demonstrate that consumption of an ethanol-containing diet for periods as short as 5 days results in relatively long-lasting alterations in avoidance behavior after withdrawal of the diet. This behavioral impairment appears to be distinct from other signs of alcohol withdrawal.
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PMID:Impairment of avoidance behavior following short-term ingestion of alcohol. 11 11

Levels of ethanol-induced conditioned taste aversion and hypothermia were found to be directly related to the concentration of fixed amounts of ethanol injected i.p. in a range of doses (1.0--1.8 g/kg) and concentrations (8--32% v/v) commonly used in behavioral studies. No effect of ethanol concentration on locomotor activity was obtained. The results of blood-ethanol determinations indicate that a given dose of ethanol is absorbed more rapidly, and thus reaches greater peak levels, when injected in a higher concentration. Thus ethanol dosage might be better manipulated by varying the volume of a single concentration rather than by altering concentration. In this way, dose-response data will not be obscured by concentration-induced differences in absorption.
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PMID:Effects of concentration of ethanol injected intraperitoneally on taste aversion, body temperature, and activity. 11 33

The results of our recent investigations have suggested that tolerance and cross-tolerance development to motor-impairing and hypothermic effects of ethanol was slowed when brain serotonin (5-HT) was extensively depleted by treatment with p-chlorophenylalanine (p-CPA). These findings have been extended by the observation that p-PCA also slowed the development of tolerance to motor-impairing effects of barbital whether tolerance was tested repeatedly in the same animal or in separate subgroups being tested only once. Additional support was provided by the demonstration that intracerebral injection of 5,7-dihydroxytryptamine (-DHT), which is known to deplete 5-HT markedly, also slowed the development of tolerance to motor-impairing and hypothermic effects of ethanol. In addition, when brain 5-HT level was elevated by administration of L-tryptophan, the rate of tolerance development to ethanol, as measured by motor impairment and hypothermia, was accelerated. In contrast to 5,7-DHT, intracerebral injection of 5,6-DHT was surprisingly found to accelerate the development of tolerance to ethanol. Upon further investigation, however, it was determined that the 5,6-DHT treatment depleted brain 5-HT levels by only 20% and, in addition, resulted in the development of supersensitivity. These results further confirm and extend the generality of our observations that 5-HT may be involved in the development of tolerance and cross-tolerance to sedatives. The possibility of a non-specific vs. specific effect of the serotoninergic system (as well as other aminergic systems) in tolerance and neuroplasticity deserves further investigation. The possible significance of these findings and the role of 5-HT (and noradrenaline) in the mechanism of tolerance are discussed in terms of analogy to enzyme or receptor mechanism.
Drug Alcohol Depend
PMID:Role of serotonin in tolerance to ethanol and barbiturates: evidence for a specific vs. non-specific concept of tolerance. 16 Aug 66

Thyrotropin-releasing hormone (TRH), administered intraperitoneally, was found to antagonize ethanol-induced sleep and hypothermia in mice without affecting brain ethanol content. This reduction of the actions of ethanol was also apparent after oral or intracisternal administration of TRH. In addition, TRH reduced ethanol-induced sleep in rats, hamsters, gerbils and guinea pigs. Evidence that the pituitary-thyroid axis is not necessary for the effects of TRH was provided by observations that hypophysectomy did not reduce TRH antagonism of ethanol narcosis and findings that neither triiodothyronine nor thyrotropin mimicked its action. Certain analogs of TRH, which have little effect on the pituitary, were also found to antagonize ethanol-induced sleep and hypothermia. Pretreatment with the antiadrenergic drugs, alpha-methyltyrosine, phentolamine and propranolol did not antagonize the ability of TRH to reduce sleep induced by ethanol. However, after intracisternal administration of atropine methyl nitrate, TRH no longer caused a significant reduction of sleep, even though TRH antagonism of the ethanol-induced hypothermia was still apparent. In contrast, central administration of other anticholinergic drugs, such as delta-tobocurarine and hexamethonium, reduced ethanol-induced sleep and this effect was additive with TRH. Carbachol also reduced ethanol sleeping time and this effect was also blocked by atropine methyl nitrate. The antagonism of ethanol-induced sleep by dibutyryl cyclic adenosine 3', 5'-monophosphate was significantly reduced but not blocked by atropine methyl nitrate. Results provide evidence that TRH has a direct extrapituitary action on brain and that both TRH and ethanol may interact with central cholinergic systems.
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PMID:Investigations into the mechanism of reduction of ethanol sleep by thyrotropin-releasing hormone (TRH). 17 53

Calcium, other divalent cations, and calcium antagonists were tested for their ability to alter ethanol-induced sleeping time, hypothermia, and behavioral intoxication in mice and rats. Calcium given intraventricularly significantly enhanced sleeping time and behavioral intoxication in a dose-related manner. The ionophores X537A and A23187 accentuated the effect of a low dose of calcium, whereas the calcium chelators EDTA and EGTA decreased sleeping time. Calcium also enhanced tertiary butanol- and chloral hydrate-induced sleeping time. The effects of cations on ethanol-induced hypothermia were less significant. The results suggest the existence of a central calcium pool that is involved in ethanol intoxication in rodents.
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PMID:Ethanol: modifications of acute intoxication by divalent cations. 34 51

The effects of 5,7-dihydroxytryptamine and L-tryptophan treatment on ethanol tolerance in the rat, as measured by the moving-belt test of motor impairment and by hypothermia, were examined in separate studies. A 2 x 2 design was used for all experiments. 5,7-Dihydroxytryptamine (200 microgram in 20 microliter CSF) or vehicle alone was administered once into both lateral ventricles of the rat. Desmethylimipramine was administered intraperitoneally prior to an intraventricular injection of 5,7-dihydroxytryptamine to prevent the destruction of norepinephrine. L-Tryptophan (75 mg/kg p.o. twice daily) or water was administered chronically. Ethanol (4--5 g/kg p.o.) or sucrose was given daily, and the development of tolerance was monitored at 5--7-day intervals. Chronic ethanol treatment produced tolerance to both the motor impairment and hypothermia effects of ethanol. 5,7-Dihydroxytryptamine and L-tryptophan treatment did not alter either the motor impairment or hypothermia produced by the initial dose of ethanol. 5,7-Dihydroxytryptamine produced a 75% depletion of brain 5-HT and slowed the development of tolerance to ethanol in both measurements. In contrast, elevation of 5-HT by L-tryptophan (39% increase by a single dose) facilitated the development of tolerance to ethanol, as seen in both measures. These findings support our hypothesis that brain 5-HT has a modulating role in the development of tolerance to ethanol.
Alcohol Clin Exp Res 1979 Oct
PMID:Effect of modification of brain serotonin (5-HT) on ethanol tolerance. 39 Oct 88


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