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  • 1
    Electronic Resource
    Electronic Resource
    Involvement of adrenergic receptor mechanisms within hypothalamus in the fever induced by amphetamine and thyrotropin-releasing hormone in the rat (1983)
    Springer
    Journal of neural transmission 58 (1983), S. 213-222 
    Details
    ISSN: 1435-1463
    Keywords: Amphetamine ; thyrotropin-releasing hormone ; fever ; aspirin ; adrenergic blockade ; thermoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 (1–10μg in 1μl) or TRH (1–4μg in 1μl) into the preoptic anterior hypothalamus caused hyperthermia or fever at the ambient temperature (Ta∶ 8, 22 and 30 °C) studied. The fever induced by d-amphetamine or TRH was due to increased metabolic heat production at Ta 8 °C, while at Ta 30 °C the fever was due to cutaneous vasoconstriction in the rat. At Ta 22 °C, the fever was due to both increased metabolism and cutaneous vasoconstriction. Furthermore, the fever induced by intrahypothalamic administration of TRH was greatly reduced by pretreatment with intrahypothalamic administration of either yohimbine (a blocking agent of alpha-adrenergic receptors), phentolamine (a blocking agent of alpha-adrenergic receptors) or DL-propranolol (a blocking agent of beta-adrenergic receptors) in the rat. However, the fever induced by d-amphetamine was antagonized by pretreatment with yohimbine or phentolamine, but not with DL-propranolol in the rat. These observations indicate that the adrenergic receptor mechanisms within the hypothalamus are involved in the fever induced by both d-amphetamine and TRH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01252807
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  • 2
    Electronic Resource
    Electronic Resource
    Endogenous pyrogen formation by human blood monocytes stimulated by polyriboinosinic acid:Polyribocytidylic acid (1993)
    Springer
    Cellular and molecular life sciences 49 (1993), S. 157-159 
    Details
    ISSN: 1420-9071
    Keywords: Monocytes ; fever ; endogenous pyrogen ; polyriboinosinic acid:polyribocytidylic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The pyrogenic response to supernatants from human blood monocytes stimulated with polyriboinosinic acid:polyribocytidylic acid (poly I:C) was characteristic of a response to endogenous pyrogen in that it was brief and monophasic, and was destroyed by heating the supernatants at 70°C for 30 min. Pyrogen production was unimpaired when the incubations were carried out in the presence of cycloheximide (50 μg/ml; an inhibitor of protein synthesis) or indomethacin (50 μg/ml; an inhibitor of prostaglandin synthesis). Also, neither interferon, interleukins, tumor necrosis factor nor prostaglandin E2 were detectable in the supernatants from the poly I:C-stimulated human monocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01989421
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  • 3
    Electronic Resource
    Electronic Resource
    Cerebral ischemia is the main cause for the onset of heat stroke syndrome in rabbits (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 225-227 
    Details
    ISSN: 1420-9071
    Keywords: Heat stroke ; fever ; cerebral blood flow ; cerebral perfusion pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract During the onset of heat stroke, rabbits displayed hyperthermia (42.8°C), and decreased cerebral perfusion pressure and decreased cerebral blood flow (as reflected by a prolonged cerebral circulation time) compared to those of normothermic rabbits. On the other hand febrile rabbits, during the fever plateau did not show the above responses, although they had a similar level of hyperthermia (42.4°C). The data support the concept that cerebral ischemia is the main cause for the onset of the heat stroke syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01930459
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  • 4
    Electronic Resource
    Electronic Resource
    Depletion of hypothalamic norepinephrine reduces the fever induced by polyriboinosinic acid: polyribocytidylic acid (Poly I:Poly C) in rats (1989)
    Springer
    Cellular and molecular life sciences 45 (1989), S. 720-722 
    Details
    ISSN: 1420-9071
    Keywords: Hypothalamus ; norepinephrine ; fever ; pyrogen ; polyriboinosinic acid ; polyribocytidylic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Administration of either Poly I:Poly C (0.05–0.50 μg) or norepinephrine (2–8 μg) into the anterior hypothalamic area produced a dose-related fever in rats. The fever induced by Poly I:Poly C was attenuated after selective depletion of norepinephrine in the hypothalamus. However, selective depletion of hypothalamic norepinephrine did not affect the fever induced by intrahypothalamic norepinephrine. The data indicate that Poly I:Poly C may act to induce fever through the endogenous release of norepinephrine from the rat's hypothalamus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01974567
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  • 5
    Electronic Resource
    Electronic Resource
    Serotoninergic mechanisms of beta-endorphin-induced hypothermia in rats (1979)
    Springer
    Pflügers Archiv 382 (1979), S. 87-90 
    Details
    ISSN: 1432-2013
    Keywords: Temperature regulation ; Beta-endorphin ; Hypothermia ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of intraventricular administration of beta-endorphin on thermoregulatory responses of unanesthetized rats to different ambient temperatures (T a ) of 8, 22 and 30°C were assessed. Administration of beta-endorphin produced a fall in rectal temperature at bothT a 8 and 22°C. The hypothermia in response to beta-endorphin was brought about by both cutaneous vasodilation (as indicated by an increase in both the tail and the foot skin temperatures) and decreases in metabolic heat production. However, atT a 30°C, administration of beta-endorphin produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermic effect induced by beta-endorphin was greatly attenuated by either the depletion of brain serotonin levels (with 5,6-dihydroxytryptamine andp-chlorophenylanine) or the blockade of opiate receptors (with naloxone). The data indicate that beta-endorphin leads to hypothermia in rats by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585909
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  • 6
    Electronic Resource
    Electronic Resource
    Stimulation of 5-hydroxytryptamine nerve cells in dorsal and median raphe nuclei elevates blood glucose in rats (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 441-445 
    Details
    ISSN: 1432-2013
    Keywords: Glucoregulation ; Serotonin ; Hypothalamus ; Electrical stimulation ; Raphe nucleus ; Kainic acid ; 5,7-Dihydroxytryptamine ; l-Glutamate ; Voltammetry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role played by dorsal or median raphe nuclei in glucoregulation was investigated by stimulating these nuclei in normal rats and in rats with chemical ablation of the hydroxytryptamine (5-HT) nerve cells in these nuclei. Electrical stimulation of either dorsal or median raphe nuclei increased blood glucose or the in vivo voltammetric signal of hypothalamic 5-OH-indole in normal rats; the increase in blood glucose level or the hypothalamic 5-OH-indole release was proportional to the intensity of stimulation. Microinjection of kainic acid or l-glutamate at the same sites also produced hyperglycemia or stimulated the hypothalamic 5-OH-indole release. This stimulation-induced hyperglycemia was significantly reduced by pretreatment of animals with spinal transection or adrenalectomy. In addition, selective destruction of the hypothalamic 5-HT nerve fibers, produced by administration of 5,7-di-hydroxytryptamine (a 5-HT nerve depletor) into both dorsal and median raphe regions, reduced the magnitude of the hyperglycemic responses to electrical stimulation of either dorsal or median raphe nuclei. The data indicate that stimulation of ascending 5-HT pathways in the rat's brain increases the adrenal-sympathetic efferent activity and leads to hyperglycemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370937
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  • 7
    Electronic Resource
    Electronic Resource
    Changes in central serotoninergic transmission affect clonidine analgesia in monkeys (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 491-495 
    Details
    ISSN: 1432-1912
    Keywords: Clonidine ; Antinociception ; Diencephalic periventricular gray ; Periaqueductal gray ; Dorsal raphe nuclei ; Serotonin ; Ketanserine ; Methysergide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of changes in central serotoninergic transmission on clonidine analgesia were assessed in monkeys. The minimum electrical current required for producing jaw opening is referred to as the pain threshold. Pain was induced by electrical stimulation of tooth pulp afferents. 2. In the first series of studies, intracerebroventricular administration of clonidine (5–30 μg) produced dose-dependent analgesia in monkeys. The clonidine-induced analgesia was abolished or attenuated by prior injection of the animals with p-chlorophenylalanine or 5,7-dihydroxytryptamine into the third cerebral ventricle. On the other hand, pretreatment of the animals by injecting 5-HT or its precursor 5-hydroxytryptophan into the cerebral ventricle potentiated the clonidine-induced analgesia in monkeys. 3. In the second series of experiments, administration of clonidine (1–10 μg) into the diencephalic periventricular gray (of the anterior hypothalamic portion), the periaqueductal gray, or the dorsal raphe nuclei also produced dose-dependent analgesia in monkeys. The analgesia induced by clonidine injection into the diencephalic periventricular gray or the periaqueductal gray was effectively antagonized by pretreatment of the animals by injecting two 5-HT receptor antagonists (such as ketanserine and methysergide) into the diencephalic periventricular gray or the periaqueductal gray. The clonidine-induced analgesia in monkeys was not affected by pretreatment of the animals with injections of either ketanserine or methysergide into the dorsal raphe nuclei. 4. The results suggest that the functional activity of central 5-HT neurons correlate well with the analgesic sensitivity of clonidine microinjected centrally. In addition, the analgesia induced by clonidine microinjected into the diencephalic periventricular gray or the periaqueductal gray was mediated by the 5-HT receptors at the site of injection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169113
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  • 8
    Electronic Resource
    Electronic Resource
    Spinal 5-HT pathways and the antinociception induced by intramedullary clonidine in rats (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 346 (1992), S. 333-338 
    Details
    ISSN: 1432-1912
    Keywords: Antinociception ; Clonidine ; Serotonin ; Spinal cord ; Medulla oblongata ; 5,7-Dihydroxytryptamine ; Cyproheptadine ; Yohimbine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible involvement of spinal 5-hydroxytryptamine (5-HT) pathways in antinociception induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata was investigated in rats. Microinjection of clonidine (10-20 µg), but not yohimbine (1 µg) or 0.9% saline, into the lateral medulla prolonged the hot plate latency in rats. This clonidine-induced antinociception was abolished by intramedullary injection of the alpha2-adrenoceptor antagonist, yohimbine. Selective destruction of spinal 5-HT neurons produced by intraspinal injection of 5,7-dihydroxytryptamine (5,7-DHT; 10 µg) or postsynaptic blockade of spinal 5-HT receptors produced by intrathecal injection of cyproheptadine (1 µg; a mixed 5-HT1/5-HT2 antagonist) also abolished clonidine-induced antinociception. Rats given 5,7-DHT intraspinally or cyproheptadine intrathecally showed a decrease in hot plate latency as compared with the controls. In anesthetized rats, the 5-HT release from the thoracic spinal cord was enhanced by microinjection of clonidine into the lateral medulla. This enhanced spinal 5-HT release evoked by intramedullary injection of clonidine was abolished by pretreatment of rats with intraspinal injection of 5,7-DHT. These results indicate that 5-HT pathways to the spinal cord mediate the antinociceptive effect induced by microinjection of clonidine into the ventrolateral surface of the medulla oblongata in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173548
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  • 9
    Electronic Resource
    Electronic Resource
    A prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the fever induced by vasopressin in the rat (1983)
    Springer
    Journal of neural transmission 56 (1983), S. 21-31 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01243371
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