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  • Articles: DFG German National Licenses  (12)
  • Thermoregulation  (9)
  • 5,7-Dihydroxytryptamine  (3)
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  • Articles: DFG German National Licenses  (12)
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  • 1
    Electronic Resource
    Electronic Resource
    Somatostatin: a hypothalamic transmitter for thermoregulation in rats (1989)
    Springer
    Pflügers Archiv 413 (1989), S. 528-532 
    Details
    ISSN: 1432-2013
    Keywords: Thermoregulation ; Hypothalamus ; Somatostatin ; Metabolism ; Vasoconstriction ; Vasodilation ; Cysteamine ; Brain ; Ambient temperature
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The changes in both the thermoregulatory responses and brain somatostatin (SS) levels produced by ambient temperature (T a) changes were assessed in rats after they had been equilibrated to each of theT a for a period of about 90 min. Cold exposure, in addition to elevating hypothalamic SS-levels, led to increased metabolism and cutaneous vasoconstriction atT a=8° C. In contrast, heat exposure, in addition to lowering hypothalamic SS-levels, resulted in decreased metabolism and cutaneous vasodilation atT a=30° C. Rats were chronically implanted with a hypothalamic cannula to allow intrahypothalamic injection of SS on the conscious rats. Direct administration of SS (0.1–0.3 μg) into the preoptic anterior hypothalamic area caused a dose-related rise in colon temperature at threeT a tested. The SS-induced hyperthermia was produced by increased metabolism atT a=8° C, whereas atT a=30° C, it was caused by cutaneous vasoconstriction. AtT a=22° C, the hyperthermia was caused by increased metabolism and cutaneous vasoconstriction. Systemic administration of cysteamine, in addition to lowering hypothalamic SS-levels, produced a dose-related fall in colon temperature atT a of 8°C and 22°C. The hypothermia induced by cysteamine was produced by decreased metabolism atT a=8° C, whereas atT a=22° C, it was caused by both decreased metabolism and cutaneous vasodilation. The data indicate that the hypothalamic SS-levels mediate normal body temperature responses in rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00594185
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    Paper (German National Licenses)
    Fulltext
  • 2
    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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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of hypothalamic noradrenaline depletion with 6-hydroxydopamine on the body temperature regulation of the rat (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 131-135 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00506192
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    Paper (German National Licenses)
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  • 4
    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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  • 5
    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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  • 6
    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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  • 7
    Electronic Resource
    Electronic Resource
    Stimulation of the nigrostriatal dopamine system inhibits both heat production and heat loss mechanisms in rats (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 346 (1992), S. 504-510 
    Details
    ISSN: 1432-1912
    Keywords: Thermoregulation ; Dopamine ; Substantia nigra ; Corpus striatum ; Voltammetry ; Medial forebrain bundle ; Metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of stimulating the pars compacta of the substantia nigra (SNC) on thermoregulation were assessed in normal rats, in rats with chemical lesion of the SNC dopamine (DA) pathways and in rats with striatal DA receptor blockade. Electrical stimulation of the SNC produced hypothermia, decreased metabolism and/or cutaneous vasoconstriction in rats at ambient temperatures (T a ) below 22°C, as well as hyperthermia and cutaneous vasoconstriction in rats at T a of 30°C. Microinjection of an excitotoxic amino acid (kainic acid) at the same brain sites also produced the same thermal responses. In vivo voltammetric studies revealed that electrical or chemical stimulation of the SNC produced an increase in striatal DA release. The enhanced striatal DA release induced by SNC stimulation was attenuated in rats after selective destruction of the nigrostriatal DA pathway by administration of 6-hydroxydopamine into the medial forebrain bundle. In addition, the magnitude of the thermal responses produced by the SNC stimulation in the cold was attenuated by selective bilateral destruction of the nigrostriatal DA pathways or selective blockade of the striatal DA produced by intrastriatal infusion of haloperidol, a DA receptor antagonist. The results indicate that stimulation of the SNC inhibits both heat production and heat loss mechanisms in the rat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169004
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  • 8
    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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  • 9
    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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  • 10
    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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