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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of narcotic analgesics on the brain 5-hydroxytryptamine (5-Ht) and 5-hydroxyindoleacetic acid (5-HIAA) levels of rats and mice were investigated in relation to our preceding data on the effect of humoral modulatorents. The results suggest that morphine accelerates the release of brain 5-HT both in rats and mice, and that neither methadone nor pethidine alters the brain 5-HT and 5-HIAA levels in rats. The morphine-induced increase in brain 5-HT turnover is likely to be involved in the morphine-induced decrease in locomotor activity and hypothermia in rats. The activity-decreasing effects of methadone or pethidine, on the other hand, are mediated by mechanisms different from those which mediate the effects of morphine. In contrast, an increase in brain 5-HT turnover in mice apparently does not play an important role on activity-increasing effects of morphine but rather participates in other pharmacological effects of morphine.
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PMID:Effects of narcotic analgesics on serotonin metabolism in brain of rats and mice. 1 94

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rate of [14C] 5-hydroxytryptamine (5-HT) from [14C]tryptophan, was significantly lower in the brainstem of the ethanol-withdrawn animals than in controls.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 It is suggested that the changes in accumulation of 14C-5-HT and 14C-5-HIAA in ethanol-withdrawn animals reflected alterations in electrical activity of serotoninergic neurons during withdrawal.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 development of tolerance to delat9-tetrahydrocannabinol (delta9-THC) was examined. Rats with permanently indwelling intravenous catheters were injected daily with delta9-THC, 2 mg/kg, for up to 10 days and on each day subjective behaviour and body weight of each rat were noted. Tolerance appeared to develop to both the excitatory and depressant behavioural effects of delta9-THC, whereas the rate of gain in body weight of delta9-THC treated rats was retarded and tolerance to this phenomenon did not develop over the experimental period. On days 1, 2, 3, 5, 6, and 10 body temperature was recorded continuously for at least 2 h after delta9-THC and in other groups of rats the brain levels of noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) were measured spectrophotofluorimetrically 1 h after delta9-THC. Tolerance developed to the delta9-THC-induced hypothermia by day 3, and on days 6 and 10 hyperthermia was observed. delta9-THC did not markedly affect the brain levels of NA or DA over the experimental period. The brain levels of 5-HT were unchanged on days 1--5 but there was a decrease on days 6 and 10. On days 1, 2, and 3 brain levels of 5-HIAA were raised, whereas on day 6 there was a decrease. These results show that delta9-THC induces tolerance to the hypothermia and elevation of brain 5-HIAA levels in a linear manner. An inverse relationship appears to exist between these two parameters.
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PMID:Relationship between body temperature and brain monoamines during the development of tolerance to delat9-tetrahydrocannabinol in the rat. 41 35

The effects of i.v. injected delta9-tetrahydrocannabinol (delta9-THC) on behaviour, body temperature and levels of brain monoamines, measured spectrophotofluorimetrically, of the rat were determined. Doses of delta9-THC in the range of 0.05--5.0 mg/kg produced biphasic changes in behaviour, body temperature and levels of 5-hydroxyindoleacetic acid (5-HIAA). The whole brain levels of dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) were not altered by delta9-THC. The subjective behavioural biphasic responses did not appear to be dose related, whereas the biphasic changes in body temperature and brain levels of 5-HIAA were dose-related. Low doses of delta9-THC (0.05 and 0.1 mg/kg) caused hyperthermia, while doses of 1.0, 2.0 and 5.0 mg/kg induced hypothermia. On the other hand, 0.05 mg/kg delta9-THC significantly reduced, whereas doses of 1.0, 2.0 and 5.0 mg/kg significantly increased the 5-HIAA levels in a dose-related manner. It is concluded that an inverse relationship exists between delta9-THC-induced changes in body temperature and alterations in brain 5-HIAA levels.
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PMID:Biphasic nature of the effects of delta9-tetrahydrocannabinol on body temperature and brain amines of the rat. 59 Mar 30

1 The effect of pretreatment with clomipramine hydrochloride (15 mg/kg, i.p.) on the (--)-trans-delta9-tetrahydrocannabinol (delta9-THC)-induced changes in body temperature and brain amines of the rat was investigated. 2 A dose of 0.05 mg/kg of delta9-THC produced hyperthermia and a decrease in whole brain concentration of 5-hydroxyindoleacetic acid (5-HIAA). Doses of 2 and 5 mg/kg produced hypothermia and increases in brain 5-HIAA whereas 0.5 mg/kg did not affect either parameter. delta9-THC, at any of the doses, did not affect the whole brain concentrations of dopamine, noradrenaline or 5-hydroxytryptamine. 3 Clomipramine modified these responses of delta9-THC in that the dose-response curves appeared to be shifted to the right. 4 It is concluded that clomipramine acts as an antagonist to these actions of delta9-THC by interfering with entry of delta9-THC into tryptaminergic neurones.
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PMID:Antagonism of the effects on thermoregulation of delta9-tetrahydrocannabinol by clomipramine in the rat. 66 19

Repeated intracisternal injections of human beta-endorphin lead to development of tolerance with respect to the catalepsy, analgesia, and hypothermia which are seen following a single injection. The initial injection of beta-endorphin results in increases in the dopamine metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in neostriatum, as well as increases in the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in hypothalamus and brainstem and a decrease in 5-HIAA in hippocampus. In the present study, we report changes in metabolism of dopamine and serotonin in specific brain areas during the development of tolerance to beta-endorphin. Thus, the development of tolerance to beta-endorphin with respect to catalepsy, analgesia, and hypothermia may be mediated by development of tolerance to the effects of beta-endorphin on brain dopamine and serotonin release.
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PMID:Alterations in brain dopamine and serotonin metabolism during the development of tolerance to human beta-endorphin in rats. 74 24

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.
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PMID:5-hydroxydopamine, unspecific centrally acting false neurotransmitter. 86 21

1. Rats were injected intravenously with 2 mg/kg (-)-trans-delta9-tetrahydrocannabinol (delta9-THC) at ambient temperatures of 4 degrees, 21 degrees, 31 degrees and 37 degrees C. 2. The general behavior exhibited by rats treated with delta9-THC was similar at all four ambient temperatures. 3. Body temperatures were recorded continuously before and after drug administration. At 4 degrees and 21 degrees C, delta9-THC caused hypothermia whereas no change in body temperature occurred at 31 degrees and 37 degrees C. 4. The concentrations in the whole brain of noradrenaline (NA), dopamine, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were determined spectrophotofluorimetrically 1 h after drug administration. At 4 degrees C delta9-THC caused an increase of 5-HT, at 21 degrees C an increase of 5-HIAA, at 21 degrees C an increase of 5-HIAA AND A decrease of NA, and at 37 degrees C an increase of 5-HT and 5-HIAA. 5. At all ambient temperatures, delta9-THC increased the brain levels of 5-HT and/or 5-HIAA. A correlation between the delta9-THC-induced hypothermic response and the possible alteration of brain 5-HT metabolism cannot be excluded.
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PMID:The effect of delta9-tetrahydrocannabinol on body temperature and brain amine concentrations in the rat at differnt ambient temperatures. 88 91

Ergometrine (EGM), 40 mg/kg ip or 100 microgram ivc, produces strong and long-lasting increase of locomotor activity of the rat, completely prevented by pretreatment with spiperone, 0.4 mg/kg, ip, or pimozide, 4 mg/kg ip. Given at a dose of 100 microgram ivc EGM produced a deep hypothermia, resistant to spiperone pretreatment (0.4 mg/kg ip). EGM decelerates cerebral serotonin (5-HT) turnover in mice and rats as measured by accumulation of 5-hydroxyindoleacetic acid after pretreatment with probenecid, and depresses the accumulation of 5-HT in the rat brain stem after pretreatment with pargyline. EGM potentiates the hind limb flexor of spinal rat. This effect is blocked by cyproheptadine (1 mg/kg ip) and danitracen (3 mg/kg ip). The results indicate that EGM stimulates both dopamine and 5-HT receptors in the central nervous system.
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PMID:Dopaminergic and serotonergic effects of ergometrine. 88 3

Compound WA-335 (9,10-dihydro-10-(-1-methyl-4-piperidylidene)9-anthrol) was studied with regard to its antidepressant and central antiserotonin action in mice and rats. WA-335 depresses reserpine-induced hypothermia, particularly in mice, but does not affect ptosis induced with this neuroleptic. The compound diminishes spontaneous motility in mice and rats, including mice stimulated with amphetamine. WA-335 acts synergistically with amphetamine in which it potentiates stereotyping and enhances motility. The compound has no influence on the action of L-DOPA and does not alter hypothermia or increase motility induced with this amino acid. WA-335 does not affect the drop in body temperature or stereotype induced with apomorphine. In mice, WA-335 inhibits motility elicited with L-5-hydroxytryptophan, and in rats as well as mice prevents occurrence of head-twitches due to activation of serotonin neurons. The compound has no effect on the righting reflex abolished with fenfluramine in frogs, and given together with reserpine slightly counteracts abolition of this reflex. WA-335 raises the level of serotonin in the brains of rats, and lowers the level of 5-hydroxyindoleacetic acid. In addition, WA-335 exhibits cholinolytic activity and abolishes the symptoms elicited with oxotremorin in mice and rats.
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PMID:The action of compound WA-335 on the central nervous system. 94 51


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