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  • 5,7-Dihydroxytryptamine  (3)
  • 5-Hydroxytryptamine  (3)
  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation of a bulbospinal 5-HT pathway in the rat brain produces hyperglycaemia (1990)
    Springer
    Pflügers Archiv 416 (1990), S. 604-608 
    Details
    ISSN: 1432-2013
    Keywords: Glucoregulation ; Spinal serotonin nerves ; Electrical stimulation ; Ventrolateral medulla ; 5,7-Dihydroxytryptamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The glucoregulatory role of spinally projecting serotonin (5-HT) neurones near the ventrolateral surface of the medulla oblongata was investigated by stimulating these nerve cells in normal rats and in rats with selective chemical ablation of 5-HT nerves in the spinal cord. Electrical stimulation of the lateral medulla produced hyperglycaemia in normal rats; the increase in blood glucose was proportional to the intensity and frequency of stimulation. Furthermore, microinjection of kainic acid or L-glutamate at the same sites also produced hyperglycaemia. This stimulation-induced hyperglycaemia was significantly reduced by spinal transection or adrenalectomy. Selective destruction of spinal 5-HT nerves produced by intraspinal injection of 5,7-dihydroxytryptamine also reduced the magnitude of the hyperglycaemia response to electrical stimulation of the lateral medulla. This indicates that stimulation of 5-HT nerve cells adjacent to the ventrolateral surface of the medulla oblongata and projecting to the spinal cord increases the adrenal-sympathetic efferent activity and leads to hyperglycaemia in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00382696
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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Effects of intracerebroventricular injection of clonidine on metabolic, respiratory, vasomotor and temperature responses in the rabbit (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1981), S. 195-201 
    Details
    ISSN: 1432-1912
    Keywords: Clonidine ; 5-Hydroxytryptamine ; Hypothermia ; Metabolic rate ; Cutaneous vasodilatation ; Respiration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The thermoregulatory outputs (including metabolic, respiratory and vasomotor activities) produced by an injection of clonidine or 5-hydroxytryptamine (5-HT) into the third cerebral ventricle of conscious rabbits were assessed at three different ambient temperatures (T a) of 2, 22 and 32°C. 2. When injected into the third cerebral ventricle, both clonidine and 5-HT produced a dose-dependent hypothermia in rabbits at both 2 and 22°C T a. The hypothermia was due to a decrease in metabolic heat production (M) at 2°C T a, while at 22°C T a the hypothermia was due to cutaneous vasodilatation. There were no changes in respiratory evaporative heat loss. 3. Furthermore, the clonidine-induced hypothermia was greatly reduced by pretreatment of the animals with either 5,6-dihydroxytryptamine (impairment of central 5-HT pathways) or yohimbine (alpha-adrenergic blocking agent), but not by 6-hydroxydopamine (impairment of central catecholamine pathways). 4. The results indicate that clonidine may act on the α-adrenergic receptors located on central 5-HT pathways to produce a hypothermic action by promoting a decrease in heat production or an increase in heat loss in the rabbit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499835
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  • 6
    Electronic Resource
    Electronic Resource
    Serotonergic mechanisms in the hypothalamus mediate thermoregulatory responses in rats (1983)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 322 (1983), S. 271-278 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00508342
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