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)

Hypothermic effects of d-Amphetamine, chlorpromazine, a variety of other phenothiazines, ET495 and haloperidol in rats at 4 degrees C were measured separately and in combination. All the drugs produced some hypothermia. Among the phenothiazines, degree of hypothermia induced was found to be correlated with relative effectiveness of the drug as an antipsychotic agent. Hypothermic effects of each of the phenothiazines in combination with d-Amphetadrugs as an antipsychotic agent. Hypothermic effects of each of the phenothiazines in combination with d-Amphetamine was greater than for either drug alone. Hypothermic effects of the combination CPZ with Amphetamine was potentiated by haloperidol but blocked by ET495. The evidence supports a model of neuronal feedback loops either within the central DA mesolimbic pathway or between the mesolimbic and nigrostriatal DA systems. The establishment of interdependency between antipsychotic and hypothermic effects of phenothiazines offers promise not only to a greater understanding of the mechanisms underlying these effects, but the possibility of an objective test for screening new materials for antipsychotic effectiveness.
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PMID:The possible role of dopamine in phenothiazine-induced hypothermia in rats: an application to DA hypothesis of schizophrenia. 1 69

Amantadine (25--100 mg kg-1, i.p.) given to rats at an ambient temperature of 4 degrees, or mice at 21 degrees, caused a marked fall in rectal temperature. Prior administration of pimozide (1--2 mg kg-1, s.c.) did not block hypothermia due to amantadine in rats or mice; in contrast, hypothermia due to apomorphine (2 mg kg-1, i.p.) and piribedil (10--40 mg kg-1, i.p.) in rats was blocked by pimozide pretreatment. Amphetamine (5 mg kg-1, i.p.) given 2 h after reserpine (2 mg kg-1, i.p.) caused a reversal of the hypothermic effect of reserpine in mice, but a reversal was not obtained with amantadine (50 mg kg-1, i.p.). Direct injection of amantadine (4--8 mg kg-1) into the cerebral ventricles (i.c.v.) of mice caused marked hypothermia which was not blocked by pimozide, but intravenous injection of the same dose of amantadine did not cause hypothermia. Rimantadine, a congener of amantadine but without anti-parkinsonian activity, also caused pimozide insensitive hypothermia in mice at doses of 50 mg kg-1, intraperitoneally or 2--4 mg kg-1, intracerebroventricularly. The main conclusion drawn from these results is that in causing hypothermia amantadine acts in the cns but not on dopamine receptors.
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PMID:The mechanism of the hypothermic effect of amantadine in rats and mice. 2 41

Drugs with the common property of stimulating dopamine receptors, have been tested for their effects on core temperature in control and reserpine-pretreated mice. Apomorphine, amantadine, amphetamine, L-dopa and atropine all produced a fall in mouse oesophageal temperature, their efficacy correlating with their ability to activate central dopamine receptors. Amphetamine and L-dopa had a biphasic effect the initial fall being followed by a rise. In reserpine-pretreated mice only amphetamine, apomorphine, L-dopa and D.L-threo-dihydroxyphenyl-serine effectively reversed hypothermia. Amphetamine had the highest efficacy of all the drugs tested. The sum of the effects of apomorphine and D.L-threo-dihydroxyphenylserine was equivalent to the effect of amphetamine alone. It is suggested that in control mice dopaminergic mechanisms mediate the hypothermia and noradrenergic mechanisms the hyperthermia. In reserpine-pretreated mice both systems are involved in the mechanisms restoring body temperature to normal.
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PMID:The role of dopamine and noradrenaline in temperature control of normal and reserpine-pretreated mice. 23 16

S-Adenosyl-L-methionine (SAM), main methyl donor, was tested in mice and rats in several models which are predictive of possible antidepressant activity. In the forced swimming test in rats the effect of SAM was compared with that of the tricyclic antidepressant amitriptyline. SAM decreased dose-dependently immobility time in the forced swimming test in mice and rats, these effects being antagonized by haloperidol and prazosin (the latter only in rats). Locomotor or exploratory activity in mice and rats was not increased by SAM. D-Amphetamine-induced locomotor hyper-activity in rats was increased by repeated (14 days, twice daily) treatment with SAM. Behavioural stimulation induced by D-amphetamine or L-dopa (given with benserazide) in mice was not changed by a single dose of SAM. The drug reduced hypothermia induced by apomorphine in mice. Hypothermia induced by reserpine or clonidine in mice was not antagonized. SAM increased the amplitude of the acoustic startle reflex. The above results indicate that the psychopharmacological profile of SAM resembles that of antidepressants in only some tests. The mechanism by which SAM produces its antidepressant effect needs further investigation.
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PMID:Antidepressant activity of S-adenosyl-L-methionine in mice and rats. 150 60

Mice selectively bred for resistance (HOT) and sensitivity (COLD) to the hypothermic effect of EtOH were tested for their hypothermic response to neurotransmitter-specific drugs and for the effect of such drugs on EtOH induced hypothermia (HT). The drugs administered were the opiate drugs morphine, levorphanol and U50488H, the dopamine agonists apomorphine, LY171535 and SKF38393, the dopamine antagonist chlorpromazine, the alpha adrenergic agonist St587, the cholinergic agonist nicotine and amphetamine, which increases the release of catecholamines. All of the drugs tested, with the exception of SKF38393 and amphetamine, induced a hypothermic response in HOT and COLD mice. SKF38393 had no effect on body temperature or HT produced by EtOH. Amphetamine caused HT at low doses and hyperthermia at high doses. COLD mice were more sensitive than HOT mice to the hypothermic effect of morphine and levorphanol, mu-opiate agonists, and U50488H, a relatively specific kappa agonist. All of the other drugs tested were approximately equally potent in HOT and COLD mice. These results suggest that the differential sensitivity of HOT and COLD mice to EtOH-induced HT may be partially mediated through genetic changes in opiate mechanisms.
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PMID:Effect of neurotransmitter-selective drugs in mice selected for differential sensitivity to the hypothermic actions of ethanol. 167 79

1. Amphetamine-induced hypothermia in mice is facilitated by dopaminergic stimulation and 5-hydroxytryptaminergic inhibition. The present study was designed to investigate: (a) the involvement of other neuronal systems, such as the gamma-aminobutyric acid (GABA), the opioid and the cholecystokinin (CCK-8) systems; (b) the possible contribution of hydroxylated metabolites of amphetamine to the hypothermia; (c) the capacity of dopamine itself to induce hypothermia and its mechanisms, in order to clarify the resistance of amphetamine-induced hypothermia to certain neuroleptics. 2. Pretreatment with the GABA antagonists, bicuculline and picrotoxin, did not inhibit amphetamine-induced hypothermia. The GABAB agonist, baclofen (2.5 mg kg-1, i.p.) potentiated this hypothermia, whereas the GABAA agonist, muscimol, did not. gamma-Butyrolactone (GBL) (40 mg kg-1, i.p.) and the neuropeptide CCK-8 (0.04 mg kg-1, i.p.) also induced potentiation. The opioid antagonist, naloxone, was without effect. 3. Dopamine itself (3, 9, 16 and 27 micrograms, i.c.v.) induced less hypothermia than the same doses of amphetamine. Sulpiride did not block dopamine-induced hypothermia, but pimozide (4 mg kg-1, i.p.), cis(z)flupentixol (0.25 mg kg-1, i.p.) and haloperidol (5 micrograms, i.c.v.) did. The direct dopamine receptor agonist, apomorphine, did not alter the hypothermia. Neither the 5-hydroxytryptamine (5-HT) receptor blocker, cyproheptadine, nor the inhibitor of 5-HT synthesis, p-chlorophenylalanine (PCPA), modified dopamine-induced hypothermia. Fluoxetine, an inhibitor of 5-HT reuptake, had no effect, whereas quipazine (6 mg kg-1, i.p.), a 5-HT agonist, totally prevented the hypothermia. Hypothermia was unaffected by pretreatment with CCK-8. 4. These data indicate that the hypothermia induced by amphetamine involves not only dopaminergic and 5-hydroxytryptaminergic systems which are functionally antagonistic, but is also facilitated by direct or indirect GABA and CCK-8 receptor stimulation. This facilitation could result, in part, from modulation of dopaminergic neurotransmission. This may explain the apparent resistance of amphetamineinduced hypothermia to some neuroleptics, while dopamine-induced hypothermia is not resistant. The possible action of hydroxylated metabolites of amphetamine may also help to explain these differences.
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PMID:Facilitation of amphetamine-induced hypothermia in mice by GABA agonists and CCK-8. 185 28

Previous studies have demonstrated anterograde amnesia (AA) and its reversal in rats trained on passive avoidance tasks. The present investigation was conducted to determine whether induction and/or reversal of AA is limited to inhibitory learning tasks or whether these phenomena can be illustrated in behavioral situations involving choice. Accordingly, in Experiment 1, rats were trained on a T-maze escape task as either hypothermic (28 degrees C) or normothermic. Twenty-four hours later half of each acquisition group was tested as either hypothermic or normothermic. Results indicated a stern retention decrement for animals trained at a lower body temperature and tested as normothermic. However, this prograde memory deficit was attenuated when animals were recooled shortly prior to testing. In an attempt to extend the phenomenon of memory recovery observed in Experiment 1, Experiment 2 examined whether pretest injections of d-amphetamine (0.5 mg/kg), a purported amnesia-attenuating agent, could lessen the AA induced by hypothermia. Amphetamine, at least at the dose used, did not reduce the memory impairment. Results are interpreted in terms of the state dependent nature of memory.
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PMID:Hypothermia-induced anterograde amnesia and its reversal in rats trained on a T-maze escape task. 372 11

1. In mice 1-10 mug histamine injected intraventricularly produces hypothermia.2. This hypothermia was not antagonized by chlorcyclizine administered subcutaneously or intraventricularly, but chlorcyclizine injected intraventricularly was effective in antagonizing the hypothermia produced by a subcutaneous injection of histamine.3. Pretreatment with atropine was without effect on the hypothermia produced by an intraventricular injection of 10 mug histamine.4. Amphetamine and tranylcypromine not only effectively reduced the intensity of, or abolished, the hypothermia but also reversed the response to an intraventricular injection of 10 mug histamine so that hyperthermia was produced. Pargyline was without effect.5. Tolazoline strongly potentiated the hypothermia produced by the intraventricular injection of 10 mug histamine, but phentolamine did not.6. It is concluded that at least part of the hypothermia produced by a subcutaneous injection of histamine arises as a result of an action on the central nervous system.7. The possible mechanisms by which histamine acting on the central nervous system produces hypothermia and the suggestion that histamine may have a physiological role in thermoregulation are discussed in the light of these findings.
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PMID:Hypothermia produced in mice by histamine acting on the central nervous system. 439 42

1. In unanaesthetized mice, weighing 20-30 g, the effect of (+)-amphetamine sulphate and p-hydroxyamphetamine hydrobromide on rectal temperature was examined. The drugs were injected intraperitoneally or into the cerebral ventricles.2. Amphetamine produced hypothermia when injected intraperitoneally in doses of 1-5 mg/kg and intraventricularly in doses of 0.5 to 25 mug. Injections of larger doses-10 mg/kg intraperitoneally and 400 mug intraventricularly-resulted in hyperthermia followed by hypothermia.3. Hydroxyamphetamine produced hypothermia only when given by the intra-ventricular route; the effect was obtained with 0.5 to 25 mug. An intraventricular injection of 200 mug resulted in hyperthermia followed by hypothermia. When injected intraperitoneally the sole effect on temperature was hyperthermia, and this response was obtained with 5 and 10 mg/kg.4. Hydroxyamphetamine injected intraperitoneally or intraventricularly in doses which produced hyperthermia reduced the noradrenaline but not the dopamine content of the brain. When injected intraventricularly in smaller doses which produced hypothermia no reduction in the noradrenaline content of the brain was obtained.5. The hypothermia is attributed to an action on the anterior hypothalamus, and the possibility is discussed that it is brought about indirectly by the release of noradrenaline. The hyperthermia on the other hand is probably a peripheral effect.
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PMID:A cntral site for the hypothermic effects of (+)-amphetamine sulphate and p-hydroxyamphetamine hydrobromide in mice. 549 94

The effects of various psychoactive drugs were studied in rats exposed for 45 min in a circularly polarized, pulsed microwave field (2450 MHz; SAR 0.6 W/kg; 2-microseconds pulses, 500 pps). Apomorphine-induced hypothermia and stereotypy were enhanced by irradiation. Amphetamine-induced hyperthermia was attenuated while stereotypy was unaffected. Morphine-induced catalepsy and lethality were enhanced by irradiation at certain dosages of the drug. Since these drugs have different modes of action on central neural mechanisms and the effects of microwaves depend on the particular drug studied, these results show the complex nature of the effect of microwave irradiation on brain functions.
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PMID:Psychoactive-drug response is affected by acute low-level microwave irradiation. 662 72


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