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 administration of TCP (15 mg/kg, i.p.) to rats pretreated with either intraperitoneal RbCl (3 mmol/kg, twice daily for 5 days) or dietary RbCl (30 mmol/kg diet, for 14 days), resulted in the complete 5-HT behavioural syndrome. Pretreatment with p-chlorophenylalanine (i.p. 300 mg/kg x2) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.) prevented the occurrence of the 5-HT syndrome, produced by dietary RbCl plus TCP. Intraperitoneal administration of RbCl had no effect upon the 5-HT behavioural syndrome, produced by 8-OH-DPAT (0.5 mg/kg, s.c.) or 5-MeODMT (2 mg/kg, i.p.) but enhanced the 5-HT syndrome produced by quipazine (20 mg/kg, i.p.), DOI (8 mg/kg, s.c.), p-chloramphetamine (4 mg/kg, i.p.) or by TCP plus L-tryptophan (50 mg/kg, i.p.) in rats. Dietary administration of RbCl resulted in the enhancement of the 5-HT2-mediated head-twitches in the mouse and the attenuation of hypothermia in the mouse, induced by 8-OH-DPAT (0.5 mg/kg, s.c.). The accumulation of 5-HT (after inhibition of monoamine oxidase) and the rate of synthesis of 5-HT in the whole brain (minus cerebellum) were enhanced by dietary and intraperitoneal administration of RbCl, respectively. The effects of lithium and rubidium, respectively, on 5HT function in brain are compared.
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PMID:The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--1. Rubidium. 138 43

It has been shown that caesium, which shares properties with quinine as a K(+)-channel blocker, enhanced 5-HT-mediated behaviour in both rats and mice. It was therefore of interest to investigate the effects of quinine on 5-HT-mediated behaviour in the rat and mouse. Quinine, dose-dependently (ED50 = 5 mg/kg), produced the 5-HT behavioural syndrome in rats pre-treated with tranylcypromine (TCP) (15 mg/kg, i.p.). p-Chlorophenylalanine (i.p., 300 mg/kg x2) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.), all prevented the behavioural syndrome induced by quinine (72 mg/kg, i.p.) plus TCP. The administration of quinine (72 mg/kg, i.p.) enhanced the 5-HT syndrome elicited by p-chloramphetamine (4 mg/kg, i.p.) and the 5-HT agonists, 8-OH-DPAT (0.5 mg/kg, s.c.), 5-MeODMT (2 mg/kg, i.p.), DOI (8 mg/kg, s.c.) and quipazine (25 mg/kg, i.p.) in rats. Pretreatment with quinine also potentiated the 5-HT2-mediated head-twitch in the mouse but had no effect on the hypothermia in the mouse, induced by 8-OH-DPAT (0.5 mg/kg, s.c.). Quinine also enhanced the rate of synthesis of 5-HT in the brain of the rat. On the basis of these findings, together with those in the preceding two papers, it is suggested that the effects of rubidium, caesium and quinine, to enhance differentially various aspects of 5-HT function are mediated by actions on 5-HT-modulated K(+)-channels. This conclusion is also discussed in relation to the actions of lithium and electroconvulsive shock on 5-HT function in brain and the treatment of manic-depressive disease.
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PMID:The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--3. Quinine. 138 54

To investigate a possible functional interaction between 5-HT1B and 5-HT1A or 5-HT2 receptors we studied the effects of 5-HT1A selective agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and gepirone, of a 5-HT1A/5-HT2 agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and of a putative 5-HT2 agonist (+/-)1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane (+/- DOI) on the 5-HT1B receptor-mediated hypothermia induced by m-trifluoromethylphenylpiperazine (TFMPP) (25 mg/kg) or m-chlorophenylpiperazine (m-CPP) (20 mg/kg) in mice. 8-OH-DPAT (1.25-5 mg/kg), gepirone (1.25-5 mg/kg), 5-MeODMT (2-8 mg/kg) and (+/-)DOI (0.5-2 mg/kg) reduced dose-dependently the TFMPP- or m-CPP-induced hypothermia. At the same time 8-OH-DPAT (2.5 and 5 mg/kg, but not 1.25 mg/kg) and gepirone (1.25-5 mg/kg) themselves decreased the body temperature in mice, while 5-MeODMT (2-8 mg/kg) and (+/-)DOI (0.5-2 mg/kg) did not affect it. The present results suggest that a functional interaction exists between 5-HT1B and 5-HT1A or 5-HT2 receptors.
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PMID:Functional interaction between 5-HT1B and 5-HT1A or 5-HT2 receptors in mice. 147 May 63

Rats and mice were given either CsCl (3 mmol/kg, s.c.) or saline (as control), twice daily for 3 days. The administration of tranylcypromine (TCP) (15 mg/kg, i.p.) to rats pretreated with CsCl produced the 5-HT behavioural syndrome. Pretreatment with CsCl also enhanced the syndrome induced by p-chloroamphetamine (3 mg/kg, i.p.) or by TCP (15 mg/kg, i.p.) plus L-tryptophan (50 mg/kg, i.p.). p-Chlorophenylalanine (300 mg/kg, i.p., daily on 2 consecutive days) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.), all prevented the behavioural syndrome induced by CsCl and TCP in rats. Pretreatment of rats with CsCl potentiated the 5-HT syndrome, elicited by the 5-HT agonists, 8-OH-DPAT (0.5 mg/kg, s.c.), 5-MeODMT (2 mg/kg, s.c.) and quipazine (25 mg/kg, i.p.). Pretreatment with CsCl potentiated the 5-HT2-mediated head-twitches in the mouse but had no effects on hypothermia in the mouse induced by 8-OH-DPAT (0.5 mg/kg, s.c.). The rate of synthesis of 5-HT in the whole brain (excluding cerebellum) was enhanced by pretreatment with CsCl. The enhancement of 5-HT neuronal function by caesium may be related to its ability to block K(+)-channels in neuronal membranes.
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PMID:The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--2. Caesium. 152 94

Many antidepressants reverse arylpiperazine-induced hypothermia after acute treatment by a mechanism that does not seem to implicate monoamine uptake inhibition. Activity is found in reversing 1-(m-trifluoromethylphenyl)piperazine (TFMPP)-induced hypothermia by desipiramine 5 and 10 mg/kg and not by maprotiline 10 and 20 mg/kg. Clomipramine and fluoxetine with comparable serotonin uptake blocking potential do not have comparable TFMPP-reversing effects. A dibenzothiadiazepine compound (IM/P/3/4), hypothesized to have antidepressant activity though devoid of uptake blocking properties, was active at 10 and 20 mg/kg. Other classes of tricyclics such as neuroleptics (clozapine 5 and 10 mg/kg) and chlorpromazine (2 and 10 mg/kg) and the H1 antihistamines, promethazine (20 mg/kg) and cyproheptadine (10 mg/kg) are active, as well as the calcium antagonists nifedipine (10 mg/kg) and verapamil (10 mg/kg). We hypothesize that properties other than monoamine-uptake block which these compounds share (such as calcium-uptake inhibition) could be involved. Activity was also seen with the 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT, at 0.05 and 0.25 mg/kg), and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT at 3 mg/kg) as well as with the muscarinic agonist oxotremorine (0.1 mg/kg).
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PMID:m-trifluoromethylphenylpiperazine and m-chlorophenylpiperazine-induced hypothermia in mice is reversed by tricyclic antidepressants and other drugs. 168 12

The repeated administration of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT, 3 mg/kg, twice daily for 14 days) significantly diminished hypothermia and corticosterone secretion induced by an acute challenge with the 5-HT1A agonist 8-OH-DPAT (0.1 mg/kg) when compared to the responses in animals treated chronically with the solvent vehicle. In contrast, the chronic administration of 5-MeODMT did not alter the magnitude of hyperthermia or corticosterone secretion induced by the acute administration of MK-212 (1.0 mg/kg). The repeated administration of the 5-HT2 agonist DOI (1.0 mg/kg, daily for 7 days) significantly reduced the increase in corticosterone, but not body temperature, produced by MK-212. Chronic treatment with DOI did not alter the hypothermia or increase in corticosterone secretion elicited by 8-OH-DPAT. These data are consistent with other evidence that these physiological effects of 8-OH-DPAT and MK-212 are mediated by 5-HT1A and 5-HT2 receptors, respectively. Thus, data presented in these studies are suggestive that the chronic administration of 5-MeODMT diminishes the responsiveness of 5-HT1A receptor-mediated changes in body temperature and corticosterone secretion without altering the responses mediated by 5-HT2 receptors. In contrast, the chronic administration of DOI selectively diminishes the magnitude of 5-HT2 receptor-mediated changes in corticosterone secretion without affecting the responsiveness of those receptors involved in thermoregulatory responses. These selective changes in receptor responsiveness following the chronic administration of these 5-HT agonists further establishes the independence of 5-HT1A and 5-HT2 receptor-mediated pharmacological effects.
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PMID:Selective cross-tolerance to 5-HT1A and 5-HT2 receptor-mediated temperature and corticosterone responses. 253 56

The effects of serotonergic agonists and antagonists on the body temperatures of rats were investigated. The administration of the serotonin (5-HT) agonist 6-chloro-2(1-piperazinyl)-pyrazine (MK-212) produced a dose-related increase in body temperature. A maximal increase in body temperature of approx. 1.1 degrees C was observed 30 min after the administration of 3 mg/kg of MK-212. In contrast, administration of the putative 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) resulted in marked, dose-related hypothermic responses. Body temperatures were decreased approx. 3 degrees C 30 min after an injection of 0.3 mg/kg of 8-OH-DPAT. Body temperatures were affected differentially by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT). Large doses (3-10 mg/kg) of 5-MeODMT elicited hyperthermic responses, whereas small doses (0.5-1.0 mg/kg) produced hypothermic responses. Treatment of rats with ketanserin (3 mg/kg) completely prevented the hyperthermic effects of 5-MeODMT, and, in fact, converted a hyperthermic response to 5-MeODMT into a marked hypothermic response. Ketanserin (0.1-1.0 mg/kg) selectively antagonized the hyperthermic response to MK-212 but did not alter the hypothermic effect of 8-OH-DPAT. Mianserin (10 mg/kg) and pirenperone (0.03 mg/kg) also selectively antagonized hyperthermia induced by MK-212. In contrast, pindolol (0.03-0.1 mg/kg) and methiothepin (10 mg/kg) selectively antagonized hypothermia induced by 8-OH-DPAT but did not alter hyperthermia induced by MK-212. Spiperone (0.1-3 mg/kg) and pizotifen (10 mg/kg) attenuated the effects of both 8-OH-DPAT and MK-212. Xylamidine, a peripheral 5-HT antagonist, had no significant effect on hyperthermia induced by MK-212 or hypothermia induced by 8-OH-DPAT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thermoregulatory responses to serotonin (5-HT) receptor stimulation in the rat. Evidence for opposing roles of 5-HT2 and 5-HT1A receptors. 295 11

The putative serotonin (5-HT)1A agonist 1-[2-(4-aminophenyl)ethyl]-4-(3-trifluormethylphenyl) piperazine (LY165163, PAPP) induces hyperphagia and hypothermia in rats, but unlike other 5-HT agonists, does not induce 5-HT stereotypy even at high doses (10 mg/kg sc). LY165163 (1 mg/kg) increased striatal DOPA accumulation in animals treated with the aromatic amino acid decarboxylase inhibitor 3-hydroxy-benzylhydrazine (NSD 1015) (100 mg/kg ip). This increase was also found when the drug was given to animals pretreated with parachlorophenylalanine (pCPA) (150 mg/kg ip daily for 3 days). LY165163 (2 and 4 mg/kg sc) inhibited stereotyped behaviour induced by the dopamine (DA) agonist apomorphine (2 mg/kg sc). LY165163 (2, 4, 10 mg/kg sc) also inhibited stereotyped components of the 5-HT syndrome induced by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT; 5 mg/kg ip) which previous studies (e.g. Andrews et al. 1982) suggested to require DA (head weaving, reciprocal forepaw treading). Thus, while other 5-HT1A agonists such as 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) cause stereotypy, this does not occur with LY165163, probably because the drug blocks DA receptors.
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PMID:Blockade of dopamine receptors explains the lack of 5-HT stereotypy on treatment with the putative 5-HT1A agonist LY165163. 295 21

The effects of the administration of L-triiodothyronine (T3) On the function of 5-HT in the CNS and its influence on the actions of electroconvulsive shock have been examined in mice. A single injection of T3 (100 micrograms/kg) had no effect 24 hr later on either 5-HT1A-mediated hypothermia, induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.5 mg/kg) or the 5-HT1B-mediated locomotor response to 5-methoxy-3-(1,2,3,6-tetrahydropyridin-4-yl) 1-H-indole (RU 24969; 50 ng i.c.v.). This treatment increased 5-HT2-induced head-twitches, produced by 5-methoxy-N,N'-dimethyltryptamine (5-MeODMT; 2 mg/kg), but did not alter 5-HT2 receptors in the frontal cortex, suggesting that this potentiation was mediated indirectly through a modulatory neurotransmitter. One injection of T3 had no effect on the concentration of 5-HT in the forebrain or mid/hindbrain, but increased 5-HIAA in the latter region. Daily injections of T3 for 10 days attenuated the responses to both 8-OH-DPAT and RU 24969. Furthermore, 5-MeODMT-induced head-twitches returned to control values and this was accompanied by a 10% decrease in 5-HT2 receptors in the cortex. Repeated administration of T3 increased levels of 5-HT in mid/hindbrain and concentrations of 5-HIAA both here and in forebrain. Hence, treatment with T3 attenuated the function of 5-HT1A and 5-HT1B receptors, but increased 5-HT2-mediated responses, although the time-courses for these effects were different. Triiodothyronine also enhanced the synthesis and turnover of 5-HT in the brain of the mouse. Repeated electroconvulsive shock (90 V, 1 sec) decreased the hypothermia induced by 8-OH-DPAT. However, 5-MeODMT-induced head-twitches were enhanced by acute and repeated electroconvulsive shock. Administration of T3 together with electroconvulsive shock did not alter the effects of electroconvulsive shock on 5-HT1A-mediated hypothermia, but markedly potentiated its actions on 5-HT2-mediated responses. These findings provide possible pharmacological evidence for the suggested antidepressant effects of T3 and the potentiation of antidepressant therapy by this thyroid hormone.
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PMID:The effects of acute and repeated administration of T3 to mice on 5-HT1 and 5-HT2 function in the brain and its influence on the actions of repeated electroconvulsive shock. 297 27

Adult rats submitted to a protein deprivation schedule at perinatal age and later rehabilitated with balanced laboratory chow were studied in order to evaluate the hypothermic effect induced by the following central agonists: apomorphine, naphazoline, clonidine, diazepam, 5-MeODMT and oxotremorine. Deprived animals showed an enhanced reactivity to the hypothermic effect of apomorphine, naphazoline and diazepam, while a reduced responsiveness to clonidine was observed. Hypothermic responses to oxotremorine and 5-MeODMT were similar between both groups. These results stressed the functional relevancy of neurochemical changes induced by early undernutrition that may persist into adult life after nutritional recovery.
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PMID:Perinatal undernutrition alters hypothermic responses to different central agonists in recovered adult rats. 362 85


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