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)

The ability of domperidone (DOM) to antagonize dopamine (DA) receptor agonist-induced hypothermia or hyperactivity was investigated in rats. Apomorphine (APO) or RDS-127 (2-di-n-propylamino-4,7-dimethoxyindane), two DA receptor agonists, produced dose-dependent hypothermia following subcutaneous (s.c.) administration. Also, RDS-127 produced hypothermia following lateral ventricular (i.c.v.) administration. The hypothermia produced by apomorphine or RDS-127 (given s.c. or i.c.v.) was antagonized by pretreatment with pimozide (0.25 mg/kg, i.p.) or domperidone (0.2, 1.0 and 5.0 mg/kg, i.p.). The hyperactivity produced by apomorphine was unaffected by pretreatment with domperidone. These data suggested that central DA receptors mediating temperature regulation, but not those mediating locomotor activity are accessible to peripherally administered domperidone. Therefore, domperidone may not be useful to differentiate hypothalamic (central) vs peripheral sites of action for DA receptor agonists in the rat.
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PMID:Is domperidone a selective peripheral dopamine-receptor antagonist in vivo? 715 11

Apomorphine (APO, 0.25 to 16 mg/kg) induced a dose dependent hypothermia in mice. Haloperidol, a dopamine antagonist, antagonized APO hypothermia due to lower doses. Clozapine and phenoxybenzamine, on the other hand, failed to modify APO hypothermia. Similarly, levopropranolol and cyproheptadine, which modify serotonergic responses, also failed to modify APO hypothermia. But fluxetine which selectively inhibits serotonin uptake, reversed APO induced hypothermia due to higher doses but not that induced by low dose of APO. The behavioral stereotypy was, however, not modified by fluoxetine pretreatment. It is concluded that APO hypothermia due to lower and higher doses are mediated by different receptors and the latter action involves the interaction of more than one type of receptor.
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PMID:Apomorphine hypothermia: interaction with serotonergic agents. 719 60

The purpose of this study was to determine the effects of a specific dopamine receptor agonist (apomorphine) and antagonist (pimozide) on thermoregulation when the heat loss pathway was activated by the stress of exercise. Apomorphine or its control vehicle (0.9% wt/vol saline) was injected systemically (0.5, 1.0, 1.5 mg/kg ip) or within the preoptic-anterior hypothalamus (5, 10, 20 micrograms) immediately before the start of treadmill exercise at 21.5 m/min. Colonic, tailskin, and ambient temperatures were recorded each minute. Oxygen consumption was calculated from on-line measurements of percent O2 and CO2. Pimozide injected systemically (0.5 mg/kg ip) had no effect on resting colonic temperature, but caused a significant (P less than 0.05) hyperthermia during treadmill exercise compared to saline controls. Central and systemic injections of apomorphine caused a dose-dependent hypothermia that was blocked by pretreatment with pimozide. Oxygen uptake values during exercise following the central injection of apomorphine were virtually identical to those following the injection of saline, but colonic temperature was significantly (P less than 0.05) lower than saline controls, indicating that the hypothermia observed was not due to a reduction in metabolic rate. These data indicate that dopamine receptors in the preoptic-anterior hypothalamus of the rat participate in the mediation of heat dissipation when the animal is challenged with a heat stress.
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PMID:Effects of apomorphine and pimozide on temperature regulation during exercise in the rat. 720 55

The purpose of this study was to determine the effects of a specific dopamine-receptor agonist (apomorphine) and antagonist (pimozide) on temperature regulation in the primate. Using 4 rhesus monkeys and 2 patas monkeys as subjects, increasing doses of apomorphine (0.05, 0.1, 0.2, 0.4, 0.6 mg/kg) injected subcutaneously produced a dose-dependent hypothermia associated with sharp elevations in tail-skin and ear pinna temperatures. Apomorphine also produced dose-related behavioral responses including salivation, hypermotility, hypersensitivity, pupil dilation and erection, suggesting a central site of action. Pre-treatment with pimozide (0.5 mg/kg, SC) blocked the apomorphine-induced hypothermia, but the subcutaneous injection of pimozide alone had no effect on body temperatures. In the patas monkey, the decline in colonic temperature following the injection of apomorphine (0.4 mg/kg) was not associated with a change in metabolic rate or heart rate. In 2 animals, mean colonic temperature fell 1.7, 0.67, and 0.3 degrees C following the injection of apomorphine ((0.4 mg/kg) in 15, 25, and 35 degrees C environments, respectively. These data suggest that the apomorphine-induced hypothermia was mediated by an increase in heat dissipation rather than a decline in heat production. The site of this drug remains to be elucidated.
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PMID:Dopamine and temperature regulation in the primate: effects of apomorphine and pimozide. 740 31

The present study explores the differential role of dopamine receptor subtypes and their interplay in the thermoregulation and stereotypic behavior in naive and acutely or chronically reserpinized rats. In naive rats, the D2 dopamine agonist B-HT920 (0.25-1 mg/kg) produced hypothermia, an effect sensitive to blockade by the D1/D2 antagonist haloperidol (0.5 mg/kg) and to potentiation by the D1 agonist SKF38393 (5 mg/kg). The hypothermic effect of the same doses of B-HT920 was reduced following acute reserpinization (5 mg/kg, 24 hr prior) but significantly enhanced following chronic reserpinization (1 mg/kg for 15 days), as compared with the B-HT920 effect in naive rats. Although SKF38393 (5 mg/kg) failed to elicit any significant effect on the rectal temperature, it potentiated the hypothermic effect of B-HT920 (0.25 mg/kg) in naive and acutely reserpinized rats. SKF38393 (5 mg/kg), on the contrary, produced a slight hyperthermia and failed to enhance the hypothermic effect of B-HT920 (0.25 mg/kg) following chronic reserpinization. A higher dose of SKF38393 (10 mg/kg), however, produced a significant rise in body temperature when administered alone or in combination with B-HT920 (0.25 mg/kg) in chronically reserpinized rats. Apomorphine (0.25-2 mg/kg), a mixed D1/D2 agonist, also produced a significant hypothermia in naive and acutely reserpinized rats. Following chronic reserpinization, however, apomorphine (0.25-1 mg/kg) produced a significant rise in body temperature, which was significantly enhanced upon co-administration with SKF38393 (5 mg/kg) but reversed to hypothermia when given in combination with B-HT920 (0.5 mg/kg). Similarly, B-HT920 (0.25-1 mg/kg) or apomorphine (0.25-2 mg/kg) produced a mild stereotypy in naive rats. The stereotypic effect of B-HT920 as well as of apomorphine was enhanced in parallel with the increase in the duration of reserpinization. SKF38393 (5 mg/kg) failed to elicit any significant stereotypic effect but significantly enhanced the stereotypic effect of B-HT920 (0.25 mg/kg) in naive or reserpinized rats. The above data, therefore, suggest a differential involvement of D2 and D1 receptors in temperature changes and stereotypy in naive and reserpinized rats, respectively.
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PMID:Differential role of dopamine receptor subtypes in thermoregulation and stereotypic behavior in naive and reserpinized rats. 790 55

1. The hydroxylated metabolites of amphetamine, p-hydroxyamphetamine (p-OHA) and p-hydroxynorephedrine (p-OHN), were administered intracerebroventricularly in mice in order to evaluate their ability to elicit hypothermia. 2. Intracerebroventricular (i.c.v.) administration of p-OHA and p-OHN (1, 3 and 9 micrograms/mouse) induced maximal hypothermia 30 min after injection. p-OHA and p-OHN (9 micrograms, i.c.v.) produced maximal decreases in rectal temperature of -6.48 +/- 0.44 degrees C and -3.82 +/- 0.42 degrees C, respectively. Both metabolites are more effective than amphetamine (at 9 micrograms, i.c.v., -3.32 +/- 0.75 degrees C). 3. Pretreatment with haloperidol (5 micrograms, i.c.v.) suppressed the fall in temperature produced by p-OHA (3 micrograms, i.c.v.) and reduced that produced by p-OHN (3 micrograms, i.c.v.), respectively. The selective dopaminergic D1 receptor antagonist, SCH 23390, and the D2 receptor antagonists, sultopride and metoclopramide, were without effect on the hypothermia induced by either metabolite. Similarly, amphetamine-induced hypothermia was only inhibited by haloperidol. Apomorphine (0.1 mg kg-1, i.p.) did not potentiate the hypothermia induced by either metabolite, whereas the selective dopaminergic D2 agonist, quinpirole (0.2 mg kg-1, i.p.) did. Amphetamine-induced hypothermia was potentiated by apomorphine and quinpirole. 4. Neither the 5-hydroxytryptamine (5-HT) receptor blocker, cyproheptadine, nor the 5-HT receptor agonist, quipazine, modified metabolite-induced hypothermia. In contrast, amphetamine-induced hypothermia was affected by these 5-HT drugs. 5. The neuropeptide CCK-8 (0.04 mg kg-1, i.p.) and gamma-butyrolactone (40 mg kg-1, i.p.) potentiated the hypothermia produced by amphetamine and its metabolites. Conversely, desipramine (20 mg kg-1, i.p.) antagonized it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Involvement of hydroxylated metabolites in amphetamine-induced hypothermia in mice. 809 41

The purpose of this study was to verify the dopamine-sensitizing behavioral effect of chronic antidepressant treatment in two selectively bred rat strains: the hypercholinergic Flinders Sensitive Line (FSL) and control Flinders Resistant Line (FRL). Two antidepressants, desipramine HCl (DMI) and sertraline HCl, were injected IP in separate groups of FSL and FRL rats in a dose of 16.5 mumol/kg twice daily for 16 days. Twenty-four hours after withdrawal, locomotor and hypothermic responses to 0.2 mg/kg of apomorphine, SC, were examined. Attenuation of the effect of apomorphine was observed in the open field: FRLs withdrawn from sertraline were significantly less mobile than control FRLs, and the same trend was found in FSL rats. Chronic DMI resulted in similar changes in the locomotor activity. Sertraline treatment decreased apomorphine-induced hypothermia by almost half in FSLs, whereas slight hyperthermia was induced in FRL rats instead. The present results suggest that in these selectively bred strains, a serotonergic antidepressant such as sertraline may have sensitized dopaminergic autoreceptors and/or desensitized postsynaptic receptors. Apomorphine-induced hypothermia could be mediated by serotonergic neuron function that may have been altered by chronic sertraline but not DMI treatment.
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PMID:Effect of chronic antidepressant treatment on responses to apomorphine in selectively bred rat strains. 822 Nov 39

The changes in DA-D2 receptor mRNA expression following apomorphine induced hypothermia and stereotypy were determined. Rectal temperatures and stereotypy were measured daily after apomorphine injection to Sprague-Dawley rats for 7 days. DA-D2 mRNA expression was determined by Northern blot analysis. Apomorphine caused a dose dependent decrease and increase in rectal temperatures and stereotypy respectively. Northern blot analysis indicated a relative abundance of the DA-D2 receptor message at the high and a reduction at the lower dose of apomorphine. The result showed that the agonist activity could influence the expression of DA-D2 receptor mRNA.
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PMID:Apomorphine induced hypothermia, stereotypy and changes in dopamine D2 mRNA expression. 834 11

Effects of prolonged lithium administration was seen on the action of various psychoactive drugs in animals. Apomorphine induced pecking in pigeons increased significantly by lithium treatment for 14 days, from 1445.3 +/- 202.5 in control to 2785.8 +/- 205.8 in Gp. B. Haloperidol-induced catalepsy score in albino rats increased significantly following chronic lithium treatment compared to control. Chlorpromazine-induced hypothermia in rabbits was immediate but transient, while in lithium treated rabbits induction of hypothermia was delayed, sustained and of greater magnitude. This action of lithium may be mediated by increasing the permeability of blood-brain barrier, or enhancing the sensitivity of alpha-adrenoceptors in brain.
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PMID:Effects of oral lithium on the action of various C.N.S. active drugs. 895 Jan 40

These studies were conducted to examine the differential response to a drug challenge under varied experimental test conditions routinely employed to study drug-induced behavioral and neurophysiological responses in rodents. Apomorphine, a nonselective dopamine agonist, was selected due to its biphasic behavioral effects, its ability to induce hypothermia, and to produce distinct changes to dopamine turnover in the rodent brain. From such experiments there is evidence that characterization and detection of apomorphine-induced activity in rodents critically depends upon the test conditions employed. In rats, detection of apomorphine-induced hyperactivity was facilitated by a period of acclimatization to the test conditions. Moreover, test conditions can impact upon other physiological responses to apomorphine such as drug-induced hypothermia. In mice, apomorphine produced qualitatively different responses under novel conditions when compared to those behaviors elicited in the home test cage. Drug-induced gross activity counts were increased in the novel exploratory box only, while measures of stereotypic behavior were similar in both. By contrast, apomorphine-induced locomotion was more prominent in the novel exploratory box. Dopamine turnover ratios (DOPAC:DA and HVA:DA) were found to be lower in those animals exposed to the exploratory box when compared to their home cage counterparts. However, apomorphine-induced reductions in striatal dopamine turnover were detected in both novel and home cage environments. The implications of these findings are discussed with particular emphasis upon conducting psychopharmacological challenge tests in rodents.
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PMID:Test conditions influence the response to a drug challenge in rodents. 1068 78


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