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

In an attempt to elucidate the possible mechanisms involved in the development of the thermoregulatory disturbances induced by systemic capsaicin treatment, the effects of 5-HT injected into the preoptic region or into the cisterna magna on the body temperature and on tail skin vasodilation were studied in control and capsaicin-treated rats. Intracisternal 5-HT elicited a comparable decrease in body temperature in both groups of animals. In contrast, intrapreoptic injection of different doses of 5-HT-induced tail skin vasodilation and hypothermia in the controls, but not in the capsaicin-treated rats. It is suggested that changes in the sensitivity of preoptic warm-responsive structures to 5-HT may contribute essentially to the specific thermoregulatory impairment brought about by systemic capsaicin treatment.
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PMID:Capsaicin impairs preoptic serotonin-sensitive structures mediating hypothermia in rats. 397 50

Pirenperone, an antagonist of 5-HT2 but not 5-HT1 receptors, has been studied for its central antiserotonergic and antidopaminergic activity. Pirenperone (0.00525-0.1 mg/kg) antagonized dose-dependently stimulation of the hind limb flexor reflex in spinal rats induced by LSD, quipazine or fenfluramine, and hyperthermia induced by serotonin (5-hydroxytryptamine; 5-HT)-like drugs (1-5-hydroxytryptophan, fenfluramine, p-chloroamphetamine, 1-/m-chlorophenyl/-piperazine, quipazine) in heat-adapted rats. Pirenperone also counteracted tryptamine-induced convulsions in rats (ID50 = 0.87 mg/kg); however, this action was weaker than that of metergoline (ID50 = 0.22 mg/kg). Pirenperone (0.1-1.6 mg/kg) produced sedation in mice and rats, and-in doses of 0.4-6.4 mg/kg-catalepsy in rats. Given in doses ranging from 0.1 to 1.6 mg/kg, pirenperone antagonized d-amphetamine-induced locomotor hyperactivity in mice and rats, the hyperactivity induced by apomorphine in rats, apomorphine- or d-amphetamine-induced stereotypy in rats and stimulation of the hind limb flexor reflex induced by the alpha-adrenoceptor agonist-clonidine. Pirenperone (6.4 mg/kg) significantly attenuated apomorphine (1 mg/kg)-induced hypothermia in mice. The results obtained indicate that pirenperone may be regarded as a relatively specific antagonist of the 5-HT2 receptor only when it is employed in very low doses (less than 0.1 mg/kg). Used in higher doses (greater than 0.1 mg/kg), it behaves like a typical neuroleptic, i.e. like a dopamine antagonist with antiserotonergic, antitryptaminergic and antiadrenergic properties.
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PMID:Central antiserotonergic and antidopaminergic action of pirenperone, a putative 5-HT2 receptor antagonist. 404 12

1. Norepinephrine (NE) and serotonin (5-HT) were simultaneously assessed in 4 discrete regions of the brain of the golden hamster. 2. Hypothalamic concentrations of both these amines are reported for the following groups: (1) normothermic controls; (2) heat acclimated; (3) cold acclimated; (4) helium-cold hypothermic; (5) rewarming; and (6) rewarmed. 3. Heat acclimated animals demonstrated approximately 35 and 25% decreases from control values for NE and 5-HT, respectively. Cold acclimated hamsters were not significantly different from controls. Helium-cold hypothermia resulted in approximately a 30 and 20% decrease in NE and 5-HT, respectively, with the latter returning to control values during rewarming. 4. The data provide indirect evidence for the involvement of NE in central pathways involving heat gain and 5-HT in pathways involving heat loss, and are discussed in terms of FELBERG & MYER'S (1964 J. Physiol., Lond. 173. 226-236) bioamine theory of thermoregulation.
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PMID:Brain norepinephrine and serotonin in the golden hamster during heat and cold acclimation and hypothermia. 612 3

The dopaminergic stimulants apomorphine and lergotrile both evoked hypothermia and stereotyped behaviour in rats. These drug effects were sensitive to antagonism by haloperidol, a dopaminergic receptor blocker. In rats pretreated with 5-hydroxytryptaminergic receptor blockers, cinanserin reduced apomorphine-induced hypothermia but cyproheptadine did not. Both cinanserin and cyproheptadine significantly potentiated lergotrile-induced hypothermia. Similarly, the stereotypic effects of apomorphine were partly reduced by cyproheptadine, although higher doses of cyproheptadine did potentiate lergotrile-induced stereotyped behaviour. These findings of different influences of 5-HT antagonists upon the effects of apomorphine and lergotrile indicate that these two dopaminergic stimulants may not work in identical manner to produce outwardly similar drug effects.
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PMID:Differential effects of 5-hydroxytryptaminergic antagonists upon apomorphine- and lergotrile-induced hypothermia and stereotyped behaviour in rats. 615 84

(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) was microinjected into the lateral brain ventricle of conscious rats in order to evaluate its pharmacological effects. Microinjection (5 microliter) were made unilaterally and the effects of AMPA were assessed for 6 hr. AMPA produced generalized myoclonic seizures, short lasting hypoactivity followed by hyperactivity and hyperthermia when low doses were injected (0.25-1.0 microgram). When AMPA was injected at higher doses (1.5-5.0 microgram) it produced generalized myoclonic seizures, a hypoactive phase and hypothermia rapidly followed by hyperthermia. As the seizure activity and hypoactive phase receded, AMPA at doses of less than 2.5 microgram produced hyperactivity and wet dog shakes in a dose-related manner. After receiving AMPA at doses of 2.5 and 5.0 microgram, rats developed transient catalepsy. High quantities (5.0 microgram) evoked a spectrum of generalized convulsive seizures lasting for 2-3 hr (1 seizure every 15 min). Biochemical assays showed that AMPA had complex effects on brain aminergic systems. AMPA decreased brain NA while brain DA concentration was slightly increased in a dose dependent manner. Moreover, AMPA increased brain 5-HT and 5-HIAA concentration in a dose- and time-related manner.
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PMID:(RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid: wet dog shakes, catalepsy and body temperature changes in rats. 617 75

In male Swiss mice, the hypothermia induced by apomorphine (10 mg/kg) was completely blocked by administration of haloperidol and d-butaclamol, but not by l-butaclamol, phenoxybenzamine, clozapine or propranolol. This substantiated the dopaminergic nature of the hypothermia induced by apomorphine. Desipramine, imipramine, chlorimipramine, fluoxetine and mazindol produced a dose-dependent blockade of apomorphine-induced hypothermia, their ED50S being 0.313, 0.733, 1.88, 6.04 and 0.0033 mg/kg, respectively. Iprindole failed to block the hypothermia induced by apomorphine. Because chlorimipramine and fluoxetine, which are relatively more selective and more potent blockers of the uptake of serotonin (5-HT) than is desipramine, were considerably less effective than the latter in antagonizing hypothermia induced by apomorphine, it was concluded that the property of blocking uptake of 5-HT alone does not contribute to the antagonism to apomorphine exhibited by the classical antidepressants. Quipazine, a 5-HT agonist, blocked the hypothermia induced by apomorphine, this effect developed tolerance on repeated administration. However, no cross-tolerance between quipazine and the antidepressants could be demonstrated. This finding provided further support for the non-involvement of 5-HT in the antagonism to apomorphine. No correlation existed between the potencies of these antidepressants to block the reuptake of norepinephrine (NE) in brain and their relative potencies to block the hypothermia induced by apomorphine. Moreover, selective depletion of high affinity binding sites for [3H]desipramine and [3H]-NE, achieved by treatment with DSP-4, failed to reduce the effectiveness of desipramine in blocking the hypothermia induced by apomorphine. Hence, inhibition of uptake of NE does not account for the antagonism by the antidepressants of apomorphine-induced hypothermia. A possibility was considered that certain antidepressants selectively blocked the hypothalamic DA receptors, thereby antagonizing the hypothermic effects of apomorphine, leaving the extra-hypothalamic dopaminergic responses of this DA agonist unaffected.
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PMID:Pharmacological studies on the antagonism by antidepressants of the hypothermia induced by apomorphine. 632 87

Neurotensin (NT), an endogenous tridecapeptide, produces significant hypothermia after intracisternal (i.c.) or intracerebroventricular (i.c.v.) administration in microgram quantities in a variety of laboratory animals. The present study sought to clarify the mechanism of the hypothermic action by utilizing pharmacological treatments which alter the function of brain neurotransmitter systems. Pretreatment of rats with anti-muscarinic (atropine), anti-noradrenergic (propranolol, a beta-blocker; phenoxybenzamine, an alpha-blocker) or anti-opiate (naloxone) agents did not significantly alter NT-induced hypothermia. Similarly depletion of brain serotonin (5-HT) with parachlorophenylalanine did not affect NT-induced hypothermia. However, depletion of brain catecholamine content with 6-hydroxydopamine resulted in a significant potentiation of NT-induced hypothermia as did pretreatment with haloperidol, a dopamine (DA) receptor antagonist. Furthermore, in rats with selective depletions of brain DA, but not norepinephrine (NE), NT-induced hypothermia was significantly augmented. Thus an interaction between brain DA systems and NT appears likely. These data indicate that NT-induced hypothermia is not dependent on intact functional activity of NE, 5-HT, muscarinic ACh or endogenous opiate systems but suggests interactions between brain DA circuits and NT. In other experiments, NT-induced hypothermia was found to be antagonized significantly by i.c. injection of thyrotropin-releasing hormone (TRH), but not by pretreatment with L-triiodothyronine. Another endogenous tripeptide (Pro--Leu--Gly--NH2, MIF-I) had no effect. Thyroidectomy (THX) significantly potentiated NT-induced hypothermia; NT administered i.c. significantly reduced the high serum TSH levels of THX rats. Thus, NT and TRH, two endogenous peptides, appear to be antagonists in certain systems.
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PMID:Neurotensin-induced hypothermia: evidence for an interaction with dopaminergic systems and the hypothalamic--pituitary--thyroid axis. 644 51

Previously it has been shown that chronic administration of p-chlorophenylalanine (p-CPA), slowed the development of tolerance to ethanol, pentobarbital and cross-tolerance development to ethanol in rats chronically treated with pentobarbital. These findings have been extended by the following observations: (1) p-CPA slowed the development of tolerance to barbital as measured by motor impairment on the moving belt test, without altering the acute response. (2) p-CPA also reduced the tolerance to barbital as measured by sleeping time, in animals chronically treated with pentobarbital. (3) Administration of L-tryptophan increased the rate of tolerance development to ethanol as measured by motor impairment and hypothermia. These results further confirm and extend the generality of our observations that 5-HT may be involved in the development of tolerance and cross-tolerance to sedatives.
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PMID:Role of serotonin (5-HT) in tolerance to ethanol and barbiturates. 644 35

The intracerebroventricular (i.c.v.) injection of taurine produced a fall in core temperature, the extent of which was dependent on the thermal gradient between the body and the environment. Concurrently, a sudden rise in ear skin temperature, which was maximal in the cold and negligible at 30 degrees C, was observed. The fever induced by i.v. injection of Escherichia coli endotoxin was antagonized by taurine. High temperatures produced by i.c.v. injection of prostaglandin E1 were also suppressed by taurine. Intracerebroventricular injections of bicuculline and strychnine, but not those of picrotoxin or pentylentetrazol, were able to reduce hypothermia induced by taurine. Intracerebroventricular injection of the taurine reuptake inhibitor guanidinoethyl sulfonate, on the contrary, did enhance the hypothermic response to taurine. Injection (i.c.v.) of serotonin (5-HT) elicited a fall in core temperature which was not accompanied by a rise in ear skin temperature, but was antagonized by the concurrent injection of the 5-HT antagonist methysergide. Pretreating animals with p-chlorophenyl-alanine caused a significant fall of brain 5-HT contents and a reduction of the hypothermic response to taurine. The latter effect was also observed when the animals were i.c.v. pretreated either the methysergide or with the 5-HT reuptake blockers chlorimipramine and Lilly 110140. These findings give support to the hypothesis that taurine-induced hypothermia in rabbits mediated by some taurine sensitive cells and, at least in part, by serotonergic synaptic mechanisms.
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PMID:Hypothermia induced in rabbits by intracerebroventricular taurine: specificity and relationships with central serotonin (5-HT) systems. 645 8

1. Either electrical stimulation of midbrain raphe nuclei or administration of 5-hydroxytryptamine (5-HT; serotonin) into the preoptic anterior hypothalamus caused hypothermia in conscious rats at ambient temperatures (Ta) of both 8 degrees C and 22 degrees C. The hypothermia was due to decreased metabolic heat production at Ta = 8 degrees C, while at Ta = 22 degrees C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at Ta = 30 degrees C, electrical stimulation of midbrain raphe or intrahypothalamic injection of 5-HT caused an insignificant change in the thermoregulatory responses. There was no changes in respiratory evaporative heat loss in response to these treatments at various Ta's. 2. Direct administration of the serotonergic receptor antagonists such as cyproheptadine and methysergide into the preoptic anterior hypothalamus caused hyperthermia in conscious rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. The hyperthermia was due to increased metabolism and cutaneous vasoconstriction. 3. The hypothermia induced by intrahypothalamic administration of 5-HT was antagonized by pretreatment with an intrahypothalamic dose of either cyproheptadine or methysergide in rats at Ta = 22 degrees C. 4. Inhibition of 5-HT neuronal activity with administration of 5-HT into the midbrain raphe regions also caused hyperthermia, increased metabolism and cutaneous vasoconstriction in rats at Ta's of 8 degrees C, 22 degrees C and 30 degrees C. 5. These observations tend to suggest that the functional activity of serotonergic receptors in the preoptic anterior hypothalamus mediates thermoregulatory responses in the rat. Activation of serotonergic receptors in the hypothalamus decreases heat production and/or increases heat loss, while inhibition of serotonergic receptors in the hypothalamus increases heat production and/or decreases heat loss in the rat.
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PMID:Serotonergic mechanisms in the hypothalamus mediate thermoregulatory responses in rats. 686 35


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