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

1. Intrahypothalamic injection of either 5-hydroxytryptamine (5-HT) (20 mug) or tryptamine (1 mug) caused hypothermia and hyperthermia respectively in lightly restrained rats maintained at an ambient temperature of 20 +/- 1 degrees C.2. Both the 5-HT- and the tryptamine-sensitive sites were located within the same region of the preoptic area.3. When rats were tested at different ambient temperatures (4, 20 and 29 degrees C), intrahypothalamic injection of 5-HT caused a marked fall in core temperature (-1.3 degrees C) in rats maintained at 4 degrees C, but smaller responses were obtained at 20 and 29 degrees C (-0.9 and -0.5 degrees C respectively). Tryptamine caused a significant hyperthermia in rats kept at 20 degrees C, but had no significant effect in rats maintained at either 4 or 29 degrees C.4. The hypothermic effect of 5-HT was selectively antagonized by systemic pre-treatment with cyproheptadine (2.5 mg/kg), but not by methergoline (0.625 mg/kg) and methysergide (0.2 mg/kg). In contrast, the hyperthermic effect of tryptamine was blocked by methergoline and methysergide, but not by cyproheptadine.5. Cyproheptadine (2.5 mg/kg) reduced the ability of rats to cope with a heat load but had no effect on the response to cold. In contrast, methergoline (0.625 mg/kg) and methysergide (0.2 mg/kg) reduced the ability to cope with cold but the rats' ability to cope with a heat load remained intact.6. These results suggest the existence of two indoleamine pathways within the preoptic anterior hypothalamus involved in the control of body temperature: a serotonergic pathway mediating heat loss and a non-serotonergic pathway mediating heat gain. The non-serotonergic system may exert its effects by modulating the activity of a central serotonergic system.
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PMID:A role for an indoleamine other than 5-hydroxytryptamine in the hypothalamic thermoregulatory pathways of the rat. 687 41

1. We have examined the effects on thermoregulation in the rat of noradrenaline bitartrate (NA), 5-hydroxytryptamine hydrochloride (5-HT) and carbamylcholine chloride (CCh) injected into the lumbar spinal subarachnoid space via a chronic indwelling catheter.2. Intrathecal injections of the monoamines and CCh reproducibly affected thermoregulation, whereas injections of control solutions had no effect.3. Intrathecal injections of NA (0.01-0.30 mumol) produced a dose-dependent hypothermia associated with a decrease in tail skin vasomotor tone. Shivering activity was not depressed during the hypothermia and sometimes increased. Intrathecal administration of the alpha-adrenergic agonist clonidine (0.0175-0.070 mumol) elicited changes in T(c) and T(sk) similar to those induced by intrathecal NA.4. Intrathecal 5-HT (0.030-0.90 mumol) elicited a dose-dependent hyperthermia accompanied by increased tail skin vasomotor tone and increased shivering.5. CCh injected intrathecally (0.001-0.06 mumol) evoked a dose-dependent hyperthermia. During the period when core temperature was rising, tail skin vasomotor tone increased and shivering-like activity was present. Once the maximum core temperature had been reached, tail skin vasodilatation occurred. Vasodilatation persisted until core temperature had returned to normal.6. Intravenous injections of 5-HT (0.30 and 0.90 mumol) or CCh (0.006 and 0.03 mumol) caused no thermoregulatory effect. The effects of these agents injected intrathecally were therefore not due to an action in the periphery.7. Intravenous infusions of NA (0.06 and 0.10 mumol) produced hypothermia and transient tail skin vasodilatation. We suggest that an action at peripheral sites may have contributed to the effects produced by intrathecal injection of this monamine.8. These findings suggest that spinal noradrenergic, serotonergic and cholinergic synapses may be importantly involved in the control of body temperature in the rat. The possible functional roles of these synapses and the putative spinal sites of action of the injected substances are discussed.
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PMID:The thermoregulatory effects of noradrenaline, serotonin and carbachol injected into the rat spinal subarachnoid space. 689 19

Direct injection of dopaminergic agonist apomorphine into the lateral cerebral ventricle, the preoptic anterior hypothalamus, the caudate-putamen complex, or the globus pallidus caused hypothermia, decreased metabolism and cutaneous vasoconstriction at ambient temperature (Ta) 8 and 22 degrees C, and hyperthermia and cutaneous vasoconstriction in the rat at Ta 30 degrees C. On the other hand, local injection of dopaminergic antagonists such as haloperidol and pimozide into the preoptic anterior hypothalamus and the striatal nuclei caused hyperthermia, increased metabolism and cutaneous vasoconstriction at Ta 8, 22, and 30 degrees C. However, there was no change in respiratory evaporative heat loss in response to administration of either dopaminergic agonist or antagonists in the rat at all Ta studied. The data indicate that hypothalamic and striatal dopaminergic receptor activation inhibits metabolic heat production in rats. In addition, intrahypothalamic injection of 5-hydroxytryptamine caused hypothermia, decreased metabolism and cutaneous vasodilatation in the rat at Ta 8 and 22 degrees C, whereas at Ta 30 degrees C caused an insignificant change in the thermoregulatory responses. Furthermore, the thermal responses induced by intrahypothalamic injection of apomorphine were not altered by depletion of hypothalamic 5-hydroxytryptamine. These observations do not support the contention that there is a dopamineserotonin link in the hypothalamic pathways that mediate heat loss mechanisms in the rat.
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PMID:Hypothalamic and striatal dopamine receptor activation inhibits heat production in the rat. 708 73

Injections of p-chloramphetamine (PCA, 5 mg/kg) induced hypothermia, ejaculation, salivation and irritability in male rats kept at an ambient temperature of 20 +/- 1 degree C. PCA-induced hypothermia was attenuated by pretreatment with the 5-hydroxytryptamine (5-HT) uptake blockers Lundbeck 10-171 (Lu 10-171, 10 mg/kg) and chlorimipramine (CMI, 20 mg/kg) and the 5-HT synthesis inhibitor parachlorophenylalanine (PCPA, 150 mg/kg daily for 3 days); it was potentiated by pretreatment with the noradrenaline uptake blocker Lundbeck 5-003 (Lu 5-003, 10 mg/kg) and the catecholamine synthesis inhibitor alpha-methyl-p-tyrosine (AMPT, 50 mg/kg every 3 hr for 9 hr). PCA- induced ejaculation was attenuated by pretreatment with Lu 10-171 and CMI. PCA-induced salivation was attenuated by pretreatment with Lu 10-171 and CMI and potentiated by pretreatment with Lu 5-003. PCA-induced irritability was potentiated by pretreatment with PCPA. These results suggest that both 5-HT and the catecholamines play a role in PCA-induced hypothermia, ejaculation, and salivation.
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PMID:Mechanisms of PCA-induced hypothermia, ejaculation, salivation and irritability in rats. 719 65

1. The thermoregulatory outputs (including metabolic, respiratory and vasomotor activities) produced by an injection of clonidine or 5-hydroxytryptamine (5-HT) into the third cerebral ventricle of conscious rabbits were assessed at three different ambient temperatures (Ta) of 2, 22 and 32 degrees C. 2. When injected into the third cerebral ventricle, both clonidine and 5-HT produced a dose-dependent hypothermia in rabbits at both 2 and 22 degrees C Ta. The hypothermia was due to a decrease in metabolic heat production (M) at 2 degrees C Ta, while at 22 degrees C Ta the hypothermia was due to cutaneous vasodilatation. There were no changes in respiratory evaporative heat loss. 3. Furthermore, the clonidine-induced hypothermia was greatly reduced by pretreatment of the animals with either 5,6-dihydroxytryptamine (impairment of central 5-HT pathways) or yohimbine (alpha-adrenergic blocking agent), but not by 6-hydroxydopamine (impairment of central catecholamine pathways). 4. The results indicate that clonidine may act on the alpha-adrenergic receptors located on central 5-HT pathways to produce a hypothermic action by promoting a decrease in heat production or an increase in heat loss in the rabbit.
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PMID:Effects of intracerebroventricular injection of clonidine on metabolic, respiratory, vasomotor and temperature responses in the rabbit. 721 68

Electrolytic lesions were made in the median, the dorsal, the dorsal + median or magnus raphe nuclei of rats. Sham-control animals were also prepared through the same procedure with the exception that no current was delivered. After 1 week of recovery from surgery, a dose-response curve to the hypothermic and motor-impairment effects (moving belt test) was carried out to assess the initial response to ethanol. The maximal fall in temperature and maximum motor impairment were used to quantify the ethanol effects. Two days after the dose-response study, hypothermia and motor impairment were again determined in all animals after a test dose of ethanol. The animals in each main treatment group were than divided into two subgroups matched on the basis of their maximum hypothermic or motor impairment response. The subgroups received daily treatment with either ethanol (5 g/kg p.o.) or calorically equivalent amounts of sucrose. Tolerance to the ethanol-induced hypothermia or motor impairment was assessed at intervals of 5 days for 25 days. Lesions of the dorsal and magnus raphe nuclei produced a negligible effect on the development of ethanol tolerance. Lesions of the median raphe nucleus delayed the development of tolerance. Combined lesions of the median + dorsal raphe nuclei did not significantly increase the effect produced by the lesions of the median raphe nuclei alone. Biochemical analysis confirmed the differential depletion of 5-hydroxytryptamine by the various lesions. These results indicate that the 5-hydroxytryptamine pathway from the median raphe nucleus to the dorsal hippocampus is important in the development of tolerance to ethanol.
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PMID:The effect of lesions in the dorsal, median and magnus raphe nuclei on the development of tolerance to ethanol. 725 52

1 Unilateral intrahypothalamic injection of 5-hydroxytryptamine (5-HT) caused a dose-related fall in core temperature in rats, whereas injection of tryptamine into the same site caused a dose-related rise in core temperature. 2 The core temperature changes induced by 5-HT or tryptamine were inhibited by intrahypothalamic pretreatment with indoleamine receptor antagonists in a dose-related manner. 3 Other neurotransmitter antagonists, haloperidol, atropine, phentolamine and (-)-propranolol, had no significant effect on core temperature changes induced by 5-HT or tryptamine. 4 A differential antagonism was observed for the indoleamine receptor antagonists against 5-HT and tryptamine-induced core temperature changes. Methergoline and triflupromazine were more selective against tryptamine-induced hyperthermia, while cyproheptadine was more selective against 5-HT-induced hypothermia. 5 Intrahypothalamic pretreatment with 5,-7-dihydroxytryptamine (5,7-DHT) 42 nmol in 2 microliter inhibited tryptamine-induced hyperthermia, but was without effect on 5-HT-induced hypothermia. 6 These results suggest the possible existence of two different receptor populations within the preoptic anterior hypothalamus in rats; one specific for 5-HT and the other for tryptamine.
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PMID:Different hypothalamic receptors mediate 5-hydroxytryptamine- and tryptamine-induced core temperature changes in the rat. 726 Apr 87

1. Intrahypothalamic injection of either dopamine or 5-hydroxytryptamine (5-HT) in a dose volume of 1 microliters caused a fall in core temperature in lightly restrained rats maintained at an ambient temperature of 17 +/- 1 degree C. 2. Haloperidol (6.5 n-mole), a dopamine antagonist, prevented the hypothermic effect of dopamine (65 n-mole), but was ineffective against the response to either intrahypothalamic 5-HT (114 n-mole) or oxotremorine (6.0 n-mole). 3. Methysergide (14 n-mole) and cryproheptadine (17 n-mole) blocked the effect of both 5-HT and dopamine. However, these same doses failed to antagonise the effect of oxotremorine. 4. Rats placed on 0.65 m below a 250 W infra-red lamp responded to the imposed heat load vasodilation of tail skin blood vessels, as indicated by an increased tail skin temperature. 5. Rats tested 2 weeks after bilateral intrahypothalamic injection of 5,6-dihydroxytryptamine (42 n-mole in 2 microliters) showed a significant reduction in their tail skin temperature response and were less able to withstand the imposed heat load. 6. Three serial sections (0.8 mm thick) were prepared from the preoptic area of the rat brain, one anterior, one posterior and one corresponding to the previously defined dopamine-sensitive site. 7. Pretreatment with 5,6-dihydroxytryptamine significantly reduced the 5-HT concentration in the dopamine sensitive site, but had no effect on the concentration of dopamine. This pretreatment blocked dopamine but not 5-HT-induced hypothermia. 8. The 5-hydroxyindoleacetic acid (5HIAA) concentration in the hypothalamus of the normal rat exposed to a heat load was found to be significantly elevated, whereas there was no change in the 5HIAA concentration in the cortex. 9. Slices of rat preoptic hypothalamus and hippocampus were incubated with [3H]5-HT (0.2-2 microM). These slices accumulated 5-HT with properties characteristic of a neuronal uptake process. 10. Perfusion with either dopamine (greater than 50 microM) or apomorphine (greater than 200 microM) enhanced the release of [3H]5-HT from the prelabelled hypothalamic slices, but failed to stimulate release from hippocampal slices. 11. The release of [3H]5-HT from preoptic slices by dopamine and apomorphine was antagonised by the dopamine antagonists haloperidol (2 microM) and (+) isomer of butaclamol (1 microM), the (-) isomer of butaclamol was inactive. 12. These results support the hypothesis of a dopamine-5HT link in the hypothalamic thermoregulatory pathways of the rat.
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PMID:A dopamine-5-hydroxytryptamine link in the hypothalamic pathways which mediate heat loss in the rat. 743 Dec 48

The effect of the atypical neuroleptic zotepine (CAS 26615-21-4), in comparison with clozapine, risperidone and haloperidol, on the responsiveness of different 5-hydroxytryptamine (5-HT1) receptor subtypes to their agonists was examined in rats and mice. The above antipsychotics were investigated in the following behavioural tests: 8-OH-DPAT (8-hydroxy-dipropylaminotetralin)-induced behavioural syndrome in rats, mCPP (mchlorophenylpiperazine)-induced hypothermia in mice and mCPP-induced hypoactivity measured in the open field in rats. Zotepine, clozapine and haloperidol did not affect the behavioural syndrome induced by 8-OH-DPAT (the selective agonist of 5-HT1A, receptor), only risperidone (used in higher doses) attenuated the effect of 8-OH-DPAT. The mCPP-induced hypothermia in mice (a 5-HT1B effect) was affected by neither zotepine nor clozapine, risperidone and haloperidol, all of them used in low doses which did not influence per se the body temperature of mice. All the tested antipsychotics given at high doses induced hypothermia in control mice; at the same time, zotepine, clozapine and risperidone attenuated the hypothermic effect of mCPP. mCPP decreases the exploratory activity of rats, this effect being considered to be mediated by 5-HT1C receptors. The tested antipsychotics, used in low doses, influenced neither the exploratory activity nor the hypoactivity induced by mCPP. When used at higher doses, they induced hypoactivity in control rats; the hypoactivity after joint administration of zotepine, risperidone or haloperidol and mCPP was significantly greater than after mCPP alone, whereas clozapine slightly attenuated the effect of mCPP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological action of zotepine and other antipsychotics on central 5-hydroxytryptamine receptor subtypes. 751 1

The time course of the effects of ethanol alone and in combination with the selective alpha 2-adrenoceptor agonist dexmedetomidine and the alpha-adrenoceptor antagonist atipamezole was studied in NIH-Swiss mice. Core body temperature, rotarod performance, motility and changes in the noradrenaline, dopamine, and 5-hydroxytryptamine (5-HT) metabolite contents of different brain parts (limbic forebrain, striatum, lower brainstem, the rest of the forebrain + midbrain and hypothalamus) were measured. Atipamezole (3 mg/kg) attenuated the hypothermia induced by either ethanol (3 g/kg) alone or ethanol in combination with dexmedetomidine (0.3 mg/kg). Atipamezole shortened the duration of the ethanol-impaired and ethanol + dexmedetomidine-impaired rotarod performance. Further, atipamezole prevented the decreased motility due to the combined treatment with ethanol and dexmedetomidine. Ethanol increased 3-methoxy-4-hydroxyphenylethylene glycol (MHPG), homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) values. Dexmedetomidine alone decreased MHPG and 5-hydroxyindoleacetic acid (5-HIAA) concentrations and increased DOPAC and HVA values. Dexmedetomidine combined with ethanol resulted in a further increase in DOPAC and HVA values. Pharmacokinetic parameters did not contribute to this antagonism of ethanol's effects by atipamezole, nor did the antagonism observed in rotarod performance or hypothermia seem to correlate with the changes seen in the brain noradrenaline and dopamine or 5-HT metabolism. In conclusion, these findings suggest that several ethanol effects are not mediated via direct activation of alpha 2-adrenoceptors, even though some of ethanol's behavioral and physiological effects may be antagonized by coadministration of alpha 2-adrenoceptor antagonists.
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PMID:The effects of ethanol in combination with the alpha 2-adrenoceptor agonist dexmedetomidine and the alpha 2-adrenoceptor antagonist atipamezole on brain monoamine metabolites and motor performance of mice. 753 79


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