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An adrenergic link in the hypothalamic pathways which mediates morphine- and beta-endorphin-induced hyperthermia in the rat.
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The mechanism underlying the hyperthermia induced by intrahypothalamic administration of either morphine or beta-endorphin has been investigated in conscious rats. Direct administration of morphine (1--8 micrograms in 1 microliter) or beta-endorphin (1--3 micrograms in 1 microliter) into the
Role of intrapreoptic norepinephrine in endotoxin-induced fever in guinea pigs.
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The peripheral administration of pyrogens has been shown previously to affect the activity of central noradrenergic neurons, but the effects have been variable and no consensus has emerged regarding their functional significance. Because norepinephrine (NE) microdialyzed into the preoptic area (PO)
Agmatine blocks morphine-evoked hyperthermia in rats.
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The present study investigated the effect of agmatine on morphine-evoked hyperthermia in rats. Morphine (4 mg/kg, s.c.) produced hyperthermia by activating mu opioid receptors. Agmatine (10 and 50 mg/kg, i.p.) was ineffective. For combined administration, agmatine decreased morphine-evoked
4-Methylthioamphetamine-induced hyperthermia in mice: influence of serotonergic and catecholaminergic pathways.
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4-Methylthioamphetamine (4-MTA), also known as p-methylthioamphetamine, is a new amphetamine derivative which in humans has been increasingly associated with severe intoxications and several deaths. As hyperthermia is considered to be one of the most life-threatening acute physiological consequences
A prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the fever induced by vasopressin in the rat.
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The effects of direct administration of vasopressin into the preoptic anterior hypothalamus on thermoregulatory functions were assessed in conscious rats at various ambient temperatures. Intrahypothalamic administration of vasopressin caused fever, increased metabolic heat production and decreased
Effects of adrenoceptor antagonists on the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha in rats.
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We investigated the effects of intraperitoneal administration of adrenoceptor antagonists to the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha (50 micrograms) injected into the third cerebral ventricle in anesthetized rats. Phentolamine inhibited the hyperthermia and hyperglycemia
Nature of hypo- and hyperthermia induced by the calcium antagonist nicardipine.
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The effects of nicardipine, a calcium channel blocking agent, injected into the cerebral ventricles, (i.c.v.), on the body temperature of unanaesthetized cats have been investigated. Nicardipine produced a biphasic effect on body temperature: a transient dose-dependent decline followed by a
Evidence that m-chlorophenylpiperazine-induced hyperthermia in rats is mediated by stimulation of 5-HT2C receptors.
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Intraperitoneal administration of m-chlorophenylpiperazine (m-CPP) to Wistar rats produced hyperthermia with a peak effect at 30 min. Pretreatment with low doses of metergoline (5-HT1/5-HT2 antagonist), mesulergine and mianserin (5-HT2C/5-HT2A antagonists) blocked m-CPP-induced hyperthermia.
Clonidine and a beta-agonists induce hyperthermia in rats at high ambient temperature.
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The effects of the alpha-agonist clonidine and the beta-agonist clenbuterol on body temperature of rats kept at high ambient temperature (28 degrees C) were studied. Both drugs induced a dose-dependent significant increase in temperature. The clonidine-induced hyperthermia was blocked by various
The autonomic stress-induced hyperthermia response is not enhanced by several anxiogenic drugs.
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While anxiety models are often based on locomotor activity responses, the stress-induced hyperthermia (SIH) paradigm uses the autonomic stress response by measuring body temperature. The effects of putative anxiogenic compounds in the SIH paradigm are inconclusive in mice and have not been examined
Involvement of adrenergic receptor mechanisms within hypothalamus in the fever induced by amphetamine and thyrotropin-releasing hormone in the rat.
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The mechanisms underlying the thermal effects induced by intrahypothalamic administration of either d-amphetamine or thyrotropin-releasing hormone (TRH) has been investigated in conscious rats. Direct administration of d-amphetamine (1-10 micrograms in 1 microliter) or TRH (1-4 micrograms in 1
Hyperthermia induced by the dopamine D1 receptor agonist SK&F38393 in combination with the dopamine D2 receptor agonist talipexole in the rat.
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The present experiments were performed to investigate the effects of dopamine D1 receptor agonists given alone or in combination with dopamine D2 receptor agonists on body temperature in rats. The selective dopamine D1 receptor agonist, 1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol
SR 95191, a selective inhibitor of type A monoamine oxidase with dopaminergic properties. I. Psychopharmacological profile in rodents.
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SR 95191 [3-(2-morpholino-ethyl-amino)-4-cyano-6-phenyl-pyridazine], a novel compound, has been shown in preliminary experiments to inhibit type A monoamine oxidase (MAO). This report describes the activities of SR 95191 in behavioral experiments in mice and rats and shows that SR 95191 has the
Psychopharmacology of midalcipran, 1-phenyl-1-diethyl-amino-carbonyl-2-aminomethylcyclopropane hydrochloride (F 2207), a new potential antidepressant.
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Midalcipran is a new potential antidepressant selected for its equipotent inhibition of noradrenaline and serotonin uptake and its lack of effect at any postsynaptic receptor. In mice it antagonized the depressant effect of tetrabenazine with an oral ED50 value of 0.5 mg/kg as compared to 2.5 mg/kg
Potentiation by TRH of the effect of imipramine on the forced-swimming test.
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Discovery of the potentiation of thyrotropin releasing hormone (TRH)-induced hyperthermia in mice by antidepressants which activate alpha-adrenergic systems instigated investigation of other relations between TRH and antidepressants. For this study the forced-swimming test using mice was chosen
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