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  • 1985-1989  (2)
  • Antinociception  (1)
  • Fever  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 608-612 
    ISSN: 1432-1912
    Keywords: Somatostatin ; Endotoxin ; Fever ; Hypothalamus ; Cysteamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary (1) The changes in rectal temperature produced by an injection of a bacterial endotoxin piromen (10–40 ng in 1.0 μl) or somatostatin-14 (SS-14; 0.1–0.3 pg in 1.0 μl) into the preoptic anterior hypothalamic area were assessed and compared in control rats, in rats with hypothalamic SS depletion, and in rats with hypothalamic SS receptor blockade. (2) Intrahypothalamic injection of either piromen or SS-14 produced a dose-related rise in rectal temperature in intact, control rats. The fever induced by intrahypothalamic injection of piromen or SS-14, as well as that induced by intraperitoneal injection of piromen, was antagonized by pretreatment of the hypothalamus with a SS-14 receptor antagonist (0.1 ng in 1.0 μl) in rats. (3) On the other hand, intraperitoneal administration of cysteamine (30–100 mg/kg), in addition to producing a dose-related fall in rectal temperature, also caused a dose-related fall in hypothalamic SS-levels in rats. Furthermore, the fever induced by intrahypothalamic injection of piromen, but not SS-14, was antagonized by depletion of hypothalamic SS levels with an intraperitoneal dose of cysteamine (30 mg/kg). (4) The results indicate that a somatostatinergic pathway in the hypothalamus may mediate endotoxin-induced fever in the rat.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 491-495 
    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
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