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  • Hypothermia  (7)
  • Serotonin  (4)
  • 5-Hydroxytryptamine  (3)
  • Dopamine  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Suppression of natural killer cell activity in mouse spleen lymphocytes by several dopamine receptor antagonists (1995)
    Springer
    Cellular and molecular life sciences 51 (1995), S. 343-348 
    Details
    ISSN: 1420-9071
    Keywords: Dopamine ; neuroleptics ; natural killer cell ; spleen lymphocytes ; interferon ; interleukin-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The effects of dopaminergic receptor inhibitors such as thiothixine (D1/D2), fluphenazine (D1/D2), trifluoperazine (D1/D2), pimozide (D2), flupenthixol (D1/D2), (+/−)-SKF 83566 (D1), and spiperone (D2) on splenic natural killer (NK) cell cytotoxic activities were assessed in vitro using mouse spleen lymphocytes or enriched NK cells. Both the activities of the splenic NK cell cytotoxicity and the effector-target cell conjugation were suppressed by thiothixine, fluphenazine, and trifluoperazine at concentrations from 2.64 to 14.78 μM. In addition, the augmentation of the cytolytic activity of NK cells induced by interferon-α or interleukin-2 was antagonized by pretreatment with these neuroleptic compounds. However, neither the splenic NK cell cytotoxicity nor the effector-target cell conjugation were affected by treatment with other neuroleptic compounds such as pimozide, flupenthixol, (+/−)-SKF 83566, and spiperone. Thus, it appears that neuroleptic compounds such as thiothixine, fluphenazine, and trifluoperazine may act through the mechanisms other than a dopaminergic pathway to affect the NK cell-target cell interaction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01928892
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  • 2
    Electronic Resource
    Electronic Resource
    Clonidine-induced hypothermia: Possible involvement of cholinergic and serotonergic mechanisms (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 124-128 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00517308
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of cholecystokinin octapeptide on thermoregulatory responses and hypothalamic neuronal activity in the rat (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1985), S. 363-367 
    Details
    ISSN: 1432-1912
    Keywords: Cholecystokinin ; Thermoregulation ; Hypothalamus ; Neuronal activity ; Metabolism ; Vasodilation ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Rats were chronically implanted with a hypothalamic cannula to allow chemical stimulation of the hypothalamus on the conscious animals in repeated experiments. Direct administration of cholecystokinin octapeptide (CCK-8) (20–60 ng) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures of 8° C and 22° C. 2. The hypothermia induced by CCK-8 was produced by a decrease in metabolism at an ambient temperature of 8° C, whereas at 22° C, it was caused by both a decrease in metabolism and an increase in cutaneous temperature. 3. However, at an ambient temperature of 30° C, intrahypothalamic administration of CCK-8 caused an insignificant change in thermoregulatory responses. Furthermore, neither intrahypothalamic injection of 0.9% saline nor intraperitoneal injection of CCK-8 (60 ng) had any effect on thermoregulatory responses at the ambient temperatures of 8°–30° C studied. 4. Under urethane anaesthesia, 59 single neurons in the preoptic anterior hypothalamic area were examined in 29 rats. Each animal was subjected to scrotal warming or cooling and to the administration of CCK-8. Microiontophoretic application of CCK-8 resulted in inhibition of the majority (75%) of cold-responsive neurons as well as excitation of the majority (77.8%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (69%) of thermally unresponsive cells were not affected by CCK-8 application. 5. The data indicate that CCK-8, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692901
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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Effects of sodium acetylsalicylate on thermoregulatory responses of rats to different ambient temperatures (1978)
    Springer
    Pflügers Archiv 378 (1978), S. 181-184 
    Details
    ISSN: 1432-2013
    Keywords: Temperature regulation ; Antipyretics ; Hypothermia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of intraperitoneal administration of sodium acetylsalicylate (aspirin) on thermoregulatory responses (Ta) of 15, 22 and 29°C were assessed. Intraperitoneal administration of aspirin produced dose-dependent hypothermia at both 15 and 22°C. The hypothermia was brought about by cutaneous vasodilation (as indicated by an increase of the tail and foot skin temperatures). However, in the heat (29°C), i. p. administration of the same amount of aspirin produced no change in rectal temperature, since the thermoregulatory responses were unaffected by aspirin application at this Ta. Thus it appears that aspirin increases heat loss and leads to hypothermia in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584454
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  • 6
    Electronic Resource
    Electronic Resource
    Intraventricular morphine produces pain relief, hypothermia, hyperglycaemia and increased prolactin and growth hormone levels in patients with cancer pain (1987)
    Springer
    Journal of neurology 235 (1987), S. 105-108 
    Details
    ISSN: 1432-1459
    Keywords: Pain ; Morphine ; Hypothermia ; Hyperglycemia ; Prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of analgesic, thermoregulatory and endocrine functions of administering morphine sulphate (0.3mg) into the lateral cerebral ventricle via an Ommaya catheter were assessed in eight patients with cancer pain. Satisfactory control of intractable pain was obtained in these patients, without any change in other sensory modalities. The delay in the onset of pain relief and the duration of analgesia ranged, respectively, from 20 to 40 min and from 12 to 16 h after drug injection. In addition, intraventricular administration of morphine caused a reduction in rectal temperature in these patients at an ambient temperature of 24°C. The hypothermia in response to the injection of morphine was due to cutaneous vasodilation and sweating. There was no change in metabolism or in respiratory evaporative heat loss after morphine injection. Further, 10 to 20 min after intraventricular administration of morphine, the blood levels of prolactin, growth hormone and glucose were elevated in these patients. The changes in temperature and endocrine levels lasted for 1–3 h. In addition to the pain relief, these side-effects of morphine treatment were short-lasting and disappeared as the morphine treatment continued. The results indicate that activation of opiate receptors in the brain produced pain relief, hypothermia (due to cutaneous vasodilation and sweating), and increased blood levels of prolactin, growth hormone and glucose in patients with cancer pain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00718020
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  • 7
    Electronic Resource
    Electronic Resource
    Paramedian reticular nucleus: a thermolytic area in the rat medulla oblongata (1990)
    Springer
    Pflügers Archiv 417 (1990), S. 418-424 
    Details
    ISSN: 1432-2013
    Keywords: Paramedian reticular nucleus ; Medulla oblongata ; Thermoregulation ; Thermolysis ; Hypothermia ; Chlorpromazine ; Pyrogen ; Fever
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of stimulation or ablation of the paramedian reticular nucleus (PRN) of the rat medulla oblongata on the thermal responses induced by ambient temperature changes, a pyrogen, or a hypothermic substance were assessed. Electrical stimulation of the PRN elicited thermolytic reactions (including decreased metabolism, cutaneous vasodilation and hypothermia) which could be mimicked by micro-injection of kainic acid (an excitotoxic amino acid) into the same region. Bilateral electrolytic lesions in the PRN prevented the animals from responding to heat stress (35° C for 30 min) to some extent, but did not prevent responses to cold stress (4° C for 60 min). In addition, the thermogenic reactions induced by intrahypothalamic injection of polyriboinosinic acid: polyribocytidylic acid (a pyrogenic substance), or the thermolytic reactions induced by intraperitoneal administration of chlorpromazine (a tranquilizer), were antagonized respectively by activation or ablation of the PRN. This suggests that the PRN of the caudal medulla may function as a thermolytic area.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370662
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  • 8
    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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  • 9
    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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  • 10
    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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