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 effects of bupropion on core body temperature of intact or reserpinized mice were studied. Intraperitoneal (IP) administration of bupropion to mice induced a dose-dependent hypothermia. The response of bupropion was decreased by the D-2 antagonist sulpiride or pimozide, but not by the D-1 antagonist SCH 23390, antimuscarinic drug atropine, alpha-adrenergic blocker phenoxybenzimine, beta-adrenergic antagonist propranolol or antiserotonergic methergoline. Reserpine induced hypothermia, which was reversed by bupropion administration. The reversal response of bupropion was reduced by propranolol, but not sulpiride, SCH 23390, phenoxybenzamine, atropine or methergoline. It is concluded that bupropion-induced hypothermia may be mediated through D-2 receptor activation, while the reversal of reserpine-induced hypothermia by bupropion may be exerted through beta-adrenergic stimulation.
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PMID:Effects of bupropion on core body temperature of mice. 134 53

The effects of dopamine agonists on core body temperature (BT) were tested in mice. Apomorphine (APO) reduced BT of the mice dose dependently. The response was inhibited by the D-2 antagonist sulpiride, but not by the D-1 antagonist SCH 23390. The D-2 agonist quinpirole also decreased BT and this was prevented by sulpiride pretreatment. Administration of the D-1 agonist SKF 38393 increased BT. This hyperthermia was decreased by SCH 23390 pretreatment. In reserpinized animals, APO caused a dose-related increase in BT. The hyperthermic response of the drug was abolished in animals pretreated with a combination of sulpiride with SCH 23390, but not by single administration of sulpiride or SCH 23390. Quinpirole and SKF 38393 caused hyperthermia in reserpinized mice. The response was decreased in animals pretreated with sulpiride or SCH 23390, respectively. BT of the intact mice was decreased, while that of reserpinized animals was increased by SCH 23390 but not by sulpiride pretreatment. It is concluded that the presynaptic dopamine neurons are involved in hypothermia, while both postsynaptic D-1 and D-2 dopamine receptors may mediated the hyperthermia induced by dopaminergic agents.
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PMID:Involvement of dopamine receptor subtypes in mouse thermoregulation. 153 46

The effect of centrally and peripherally administered dopamine D1 and D2 specific compounds on core body temperature in mice was investigated. Quinpirole (LY-17155), a D2 agonist, induced a dose-dependent fall in body temperature (2.4-11.6%; p less than 0.003) when injected intraperitoneally (ip, 0.3-3.0 mg/kg) and intracerebroventricularly (icv, 0.1 mg/kg). This quinpirole-induced (1.0 mg/kg, ip) hypothermia was reversed by the central and peripheral administration of the D2 antagonists S-(-)-sulpiride (3.0-30.0 mg/kg, ip; 0.1-3.0 mg/kg, icv) and spiperone (0.03 and 0.1 mg/kg, ip; 0.03-3.0 mg/kg, icv). Domperidone, a D2 antagonist which does not cross the blood brain barrier, had no effect on quinpirole-induced hypothermia (1.0-10.0 mg/kg, ip). Domperidone partially reversed quinpirole-induced hypothermia at 0.1-30.0 mg/kg, icv. The D1 agonist, SKF-38393 at a high dose of 10.0 mg/kg, ip mildly attenuated quinpirole-induced hypothermia (a 1.8% increase in temperature). SKF-38393 at 10.0 mg/kg, icv potentiated quinpirole-induced hypothermia. SCH-23390 (0.1-3.0 mg/kg, ip), a D1 antagonist, had no effect on quinpirole-induced hypothermia and potentiated the hypothermia when administered icv. An ineffective icv dose of spiperone (0.01 mg/kg) in reversing quinpirole-induced hypothermia was rendered effective by prior administration of SCH-23390 (0.1-3.0 mg/kg, icv) but not by SKF-38393 (1.0-10.0 mg/kg, icv). These data suggest a central D2 receptor mechanism mediating hypothermia in mice which is capable of being modulated by the D1 receptor.
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PMID:Dopamine D2-receptors mediate hypothermia in mice: ICV and IP effects of agonists and antagonists. 168 37

In mice, rendered poikilothermic by a prior (18 hr) subcutaneous administration of reserpine (3 mg/kg), the subcutaneous administration of apomorphine increased dose-dependently the body temperature. This effect was potentiated by the specific D2 dopamine antagonist sulpiride. On the contrary, it was reduced by the specific D1 dopamine antagonist SCH 23390. A desensitization of D2 receptors was produced by the repeated administration of the specific D2 agonist RU 24926. This pretreatment led to an increased efficacy of apomorphine in antagonizing reserpine-induced hypothermia. Similarly, a desensitization of D1 receptors was created by the repeated administration of the specific D1 agonist CY 208-243. This pretreatment significantly diminished the efficacy of apomorphine in antagonizing reserpine-induced hypothermia. The repeated administration of the D1 agonist CY 208-243, in non-reserpinized mice, significantly increased the hypothermic effect of apomorphine (1 mg/kg). Thus, it appears that, in normal mice, but especially in reserpinized mice, the stimulation of D1 receptors by apomorphine induces an increase in body temperature that is masked, especially in normal mice, by the hypothermic effect, resulting from the simultaneous stimulation of D2 receptors.
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PMID:Dopamine D1 and D2 receptors mediate opposite effects of apomorphine on the body temperature of reserpinized mice. 196 37

In naive mice, the selective D1 agonist, SK&F 38393 (7.5-30 mg/kg s.c.), induced a significant rise of body temperature (0.5-1 degree C) which was antagonized by SCH 23390 (100 micrograms/kg s.c.) and by flupenthixol (0.4 mg/kg i.p.). In mice treated with reserpine (5 mg/kg s.c.) 18 h before testing, which on its own caused intense hypothermia (10-12 degrees C), SK&F 38393 (1.87-30 mg/kg s.c.) induced a dose-dependent and more marked rise of body temperature (5-7 degrees C). Similarly, SK&F 38393 (30 mg/kg s.c.) partially prevented reserpine-induced hypothermia. The central origin of the SK&F 38393 effects in reserpine-treated mice is indicated by the rise of body temperature induced by the i.c.v. administration of the drug (12.5-50 micrograms per mice). The SK&F 38393-induced rise of body temperature in acutely reserpinized mice was antagonized by SCH 23390 (50-200 micrograms/kg s.c.), clozapine (1.87-30 mg/kg i.p.) or chlorpromazine (2-32 mg/kg i.p.) but not by metoclopramide (25 or 100 mg/kg i.p.) or amisulpride (12.5 or 50 mg/kg). In naive mice, apomorphine (1 mg/kg s.c.) or LY 171555 (0.4 mg/kg s.c.) induced hypothermia which was antagonized by amisulpride (12.5 mg/kg i.p.); a transiently increased body temperature was even measured 30 min after apomorphine injection in amisulpride-treated mice. Apomorphine (1 mg/kg s.c.) induced a rise of body temperature in acutely reserpinized mice which was significantly reduced by SCH 23390 (50 and 200 micrograms/kg s.c.) and significantly increased by amisulpride (12.5 and 50 mg/kg i.p.). These data suggest that pharmacologically different dopamine receptor subtypes mediate different effects on body temperature in mice: D1 dopamine receptors mediate a rise of body temperature which is increased in hypothermic reserpinized animals and dopamine receptors of the D4 subtype mediate the decrease of body temperature in naive mice.
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PMID:The rise of body temperature induced by the stimulation of dopamine D1 receptors is increased in acutely reserpinized mice. 197 57

The reversal of hypothermia, induced by reserpine or by a high (16 mg) dose of apomorphine, in male Swiss mice, does not seem to utilize a common mechanism. Desipramine (20 mg kg-1 i.p., 60 min) or nortriptyline (8 mg kg-1 i.p., 60 min) increased temperature in both reserpine (2.5 mg kg-1 s.c., 18-19 h) and apomorphine (16 mg kg-1 s.c., 30 min) treated mice. In apomorphine-treated animals the effect of both drugs was reversed by the mixed dopaminergic D1- D2-antagonist haloperidol (1 mg kg-1 i.p., 90 min), the D1-receptor blocking drug SCH 23390 (0.05 mg kg-1 s.c., 30 min), the alpha 1-adrenoceptor blocking drugs prazosin (3 mg kg-1 s.c., 90 min) and phenoxybenzamine (20 mg kg-1 i.p., 65 min), the beta-adrenoceptor blocking drug (+/-)-propranolol (10 mg kg-1 i.p., 120 min), and the opioid antagonist naloxone (2 mg kg-1 i.p., 15 min). In contrast the selective D2-antagonist (+/-)-sulpiride (100 mg kg-1 i.p., 90 min), and the alpha 2-antagonist yohimbine (2 mg kg-1 i.p., 75 min), failed to effect the reversal of apomorphine hypothermia brought about by desipramine or nortriptyline. Their temperature effects in reserpinized mice were not modified by any of the antagonists tested.
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PMID:Desipramine and nortriptyline antagonize apomorphine and reserpine hypothermia by a different mechanism. 198 90

We have studied the behavioral responses in open-field and the changes in body temperature induced after chronic treatment with a selective D1 antagonist, SCH 23390, a selective D2+ antagonist, sulpiride, or a non specific but preferential D2 antagonist, haloperidol. After chronic treatment with SCH 23390 or sulpiride, rats were challenged with SKF 38393, selective D1 agonist, or LY 171555, selective D2 agonist, in order to study the responses of D1 and D2 stimulation. After chronic SCH 23390, an increase of the locomotion and of the number of rears were observed whereas, no changes were induced by chronic sulpiride or haloperidol. Acute treatment with sulpiride blocked the hyperlocomotion induced by chronic SCH 23390. In naive rats acute administration of SKF 38393 or LY 171555 did not produce any change in locomotion or rearing. In rats treated chronically with SCH 23390 this acute administration of LY 171555 induced an increase of the number of squares and of the number of rears. In these animals, acute administration of SKF 38393 also augmented the number of squares crossed. In contrast, chronic sulpiride did not modify behavioral responses obtained after acute SKF 38393 or LY 171555. Colonic temperature was not changed after acute SKF 38393 while acute LY 171555 induced a hypothermia. Chronic sulpiride did not modify the responses of SKF 38393 or LY 171555, but an increase in body temperature was observed after acute SKF 38393 in animals chronically treated with SCH 23390. The present results support a different behavioral expression of D1 and D2 supersensitivity in rats. Furthermore, chronic treatment with a D1 antagonist induced facilitatory effects on D2 behavioral responses; however, these D1-D2 interactions were not observed in body temperature responses.
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PMID:Effects induced by chronic treatment with selective D1 or D2 antagonists on open-field behavior and colonic temperature. 214 27

The effects of surgical adrenalectomy were investigated on behavioural responses produced by the selective D-1 agonist, SK&F 38393, alone, and in combination with the D-2 agonist, quinpirole (LY171555). Further, stereotyped responses to apomorphine and LY171555 were assessed following treatment with either the D-1 or the D-2 antagonists, SCH 23390 and raclopride, respectively. There was no difference between sham-adrenalectomized (sham) and adrenalectomized (ADX) groups in responses to SK&F 38393. Although concomitant stimulation of both receptor subtypes increased the incidence of stereotyped sniffing behaviour, there was no difference in the magnitude of this effect between the sham and ADX groups. Raclopride reduced LY171555-induced sniffing and hypothermia less in ADX rats than in sham controls, which was consistent with the hypothesis that adrenocortical hormones affect D-2 receptor responsiveness. SCH 23390 had a greater inhibitory effect on LY171555 responses, but a smaller effect on apomorphine responses in the ADX group compared with their sham controls. It is concluded that the amplified D-2-stimulated response observed in ADX rats may be more dependent on tonic D-1 receptor activation than the control D-2 response of shams.
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PMID:Effects of adrenalectomy on responses mediated by dopamine D-1 and D-2 receptors. 256 98

The nonselective dopamine (DA) receptor agonists R(-)apomorphine (APO) and R(-)-N-n-propylnorapomorphine (NPA) elicited dose- and time-dependent hypothermia in mice with ED50 values of 300 and 18 micrograms/kg, respectively. The selective D2 agonist quinpirole (LY 171555) also elicited dose-dependent hypothermia, whereas the selective D1 agonist SKF 38393 had no effect. The selective D1 and D2 antagonists SCH 23390 (1 mg/kg) and sulpiride (200 mg/kg), respectively, did not significantly alter body temperature. The hypothermic effect of a maximal dose of NPA (0.2 mg/kg) was not blocked by SCH 23390 (1 mg/kg) but was significantly attenuated (p less than 0.001) by pretreatment with sulpiride (200 mg/kg). Pretreatment with sulpiride (200 mg/kg) produced a parallel, 40-fold shift to the right of the dose-response curve for NPA. Partial, irreversible DA receptor inactivation by N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) (2 mg/kg) reduced the maximal hypothermic effect of NPA (to 49% of control) without altering its ED50. Analysis of the data indicated a linear relationship between DA receptor occupancy and hypothermic response. The results demonstrate that DA agonist-induced hypothermia in mice is mediated by D2 receptors and that there is no receptor reserved for this response.
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PMID:Hypothermia in mice: D2 dopamine receptor mediation and absence of spare receptors. 256 21

In mice rendered poikilothermic by a prior (18 h) subcutaneous administration of reserpine (3 mg/kg) the injection of the D1 dopamine agonist SKF 38393 in doses of 1 mg/kg or more increased dose-dependently, the body temperature. The D1 dopamine antagonist SCH 23390, administered subcutaneously, antagonized, with an ID50 of 16 micrograms/kg, the reversal by SKF 38393 of reserpine-induced hypothermia. The intracerebroventricular administration of 1 microgram per mouse of SKF 38393 was sufficient to elevate by about 7 degrees C the temperature of reserpinized mice. It is concluded that stimulation of central D1 dopamine receptors leads to a marked reversal of reserpine-induced hypothermia; this may constitute a new test to investigate interaction of drugs with these receptors. In reserpine-pretreated mice, the dopamine (DA) agonist apomorphine, which stimulates both the D1 and D2 subtypes of DA receptors, increases body temperature according to a mechanism insensitive to the specific D2 DA antagonist sulpiride (Horowski 1978) or the preferential D2 DA antagonist haloperidol (Danielson, Coutts, Keashly and Tang 1985). This observation led us to believe that D1 DA receptors could be involved in the reversal of the hypothermia induced by reserpine. To check more directly the involvement of D1 DA receptors in the reversal of the reserpine-induced hypothermia we have tested the specific D1 agonist SKF 38393 (Setler, Sarau, Zirckle and Saunders, 1978), administered peripherally or intracerebroventricularly and we have studied its interaction with the specific D1 antagonist SCH 23390 (Iorio, Barnett, Leitz, Houser and Korduba, 1983).
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PMID:Stimulation of central D1 dopamine receptors reverses reserpine-induced hypothermia in mice. 256 97


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