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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 257-269 
    ISSN: 1435-1463
    Keywords: Thermoregulation ; db cyclic AMP ; hypothermia ; hyperthermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of intraventricular administration of dibutyryl adenosine 3′, 5′-cyclic monophosphate (db cyclic AMP) on the thermoregulatory responses of unanesthetized rats and rabbits to different ambient temperatures (Ta) were assessed. Administration of db cyclic AMP (10–60 mM) produced dose-dependent hypothermia in both rats and rabbits at Ta 2–22 °C. The hypothermia in response to db cyclic AMP was due to decreased metabolic heat production and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. In contrast, in the heat (30–32 °C), db cyclic AMP administration produced dose-dependent hyperthermia in these animals. The hyperthermia was due to increased metabolism (due to muscular shivering) and decreased heat losses. The reduction in heat losses was shown by a decrease in both cutaneous circulation and respiratory evaporative heat loss. The data demonstrate that the thermoregulatory responses induced by central administration of db cyclic AMP are Ta-dependent.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 124-128 
    ISSN: 1432-1912
    Keywords: Clonidine ; Hypothalamus ; 5-Hydroxytryptamine ; Acetylcholine ; Thermoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The thermoregulatory effects (including metabolic, vasomotor and respiratory activities) produced by an injection of clonidine (1–3 μg in 0.5 μl) into the preoptic anterior hypothalamus were assessed in conscious rats at ambient temperatures (T a) of 8, 22 and 30°C. 2. Intrahypothalamic administration of clonidine caused a dose-dependent fall in rectal temperature at T a 8°C and 22°C. The hypothermia in response to clonidine was due to decreased metabolic heat production and/or cutaneous vasodilation. There was no change in respiratory evaporative heat loss. 3. The clonidine-induced hypothermic response was attenuated by pretreatment of the rats with either 5,7-dihydroxytryptamine (10 μg, administered intrahypothalamicly, 14 days before clonidine injection), yohimbine (0.2 μg, administered intrahypothalamicly, 10 min before clonidine injection), cyproheptadine (1 μg, administered intrahypothalamicly, 10 min before clonidine injection), or atropine (0.1 μg, administered intrahypothalamicly, 10 min before clonidine injection). 4. The data indicate that clonidine may act on α-adrenoceptors located on a serotonin-acetylcholine pathway within the preoptic anterior hypothalamus to induce hypothermia by promoting a reduction in metabolic heat production and/or an enhancement in dry heat loss in rats.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 322 (1983), S. 271-278 
    ISSN: 1432-1912
    Keywords: 5-Hydroxytryptamine ; Hypothalamus ; Thermoregulation ; Raphe nucleus ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 (T a) of both 8° C and 22°C. The hypothermia was due to decreased metabolic heat production at T a=8°C, while at T a=22°C the hypothermia was due to both decreased metabolism and increased heat loss (cutaneous vasodilatation). However, at T a=30°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 T a'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 T a's of 8°C, 22°C and 30°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 T a=22°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 T a's of 8°C, 22°C and 30°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.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 131-135 
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Hypothalamus ; Dopamine ; Thermoregulation ; 6-Hydroxydopamine ; Hyperthermia ; Metabolism-vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Rats which had been pretreated with 3 intrahypothalamic doses of 10 μg of 6-hydroxydopamine (6-OHDA) to cause a selective depletion of hypothalamic noradrenaline to 26.7% of control hypothalamic noradrenaline maintained rectal temperature within the normal limits displayed by the control group. However, noradrenalinedepleted rats displayed a decrease in both cutaneous temperature and metabolic heat production in the cold (8°C). 2. Intrahypothalamic injections of 6-OHDA in normal rats at room temperature (22°C) caused an acute hyperthermia of up to 1.1°C which lasted for about 6 h. The acute hyperthermia in response to 6-OHDA was due to both cutaneous vasoconstriction and increased metabolism in the rat. Selective depletion of hypothalamic noradrenaline without affecting hypothalamic dopamine by prior treatment with 6-OHDA markedly reduced the hyperthermic responses to a subsequent dose of 6-OHDA. Therefore, the acute hyperthermic responses to 6-OHDA may be related to a release of noradrenaline in the hypothalamus. 3. The data indicate that activation of noradrenergic pathways in the hypothalamus facilities heat production and inhibits heat loss mechanisms in the rat.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 56 (1983), S. 21-31 
    ISSN: 1435-1463
    Keywords: Thermoregulation ; fever ; hypothalamus ; vasopressin ; adrenergic receptors ; aspirin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 heat loss (cutaneous vasoconstriction) in rats. There was no changes in respiratory evaporative heat loss in response to administration of these drugs. Furthermore, it was found that the fever reactions induced by intrahypothalamic vasopressin was antagonized by pretreatment of animals with an intrahypothalamic dose of either yohimbine (an alpha-adrenergic receptor antagonist), propranolol (a beta-adrenergic receptor antagonist), or sodium acetylsalicylate (a prostaglandin synthetase inhibitor). The data indicate that a prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the vasopressin-induced fever in rats.
    Type of Medium: Electronic Resource
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