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  • 1995-1999  (2)
  • 5-HT transporter  (1)
  • Key words Glucocorticoids  (1)
  • 82.50
  • 1
    Electronic Resource
    Electronic Resource
    Long-term modulation of presynaptic 5-HT-output: Experimentally induced changes in cortical 5-HT-transporter density, tryptophan hydroxylase content and 5-HT innervation density (1997)
    Springer
    Journal of neural transmission 104 (1997), S. 993-1004 
    Details
    ISSN: 1435-1463
    Keywords: [3H]-paroxetine-binding ; tryptophan hydroxylase ; serotonin (5-HT) ; 5-HT transporter ; 5-HT innervation ; food restriction ; bulbectomy ; amphetamines ; antidepressants ; presynaptic regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Whereas experimentally induced long-term changes of postsynaptic mechanisms of 5-HT neurotransmission have been studied in great detail, much less is currently known about the effects of certain treatments on the presynaptic components governing the output of 5-HT in individual brain regions. This contribution summarizes the results of a series of experiments on the influence of different physiologic and pharmacologic manipulations on three different parameters of 5-HT presynapses, 5-HT transporter density, tryptophan hydroxylase content, and serotonin level in the rat frontal cortex. The combined measurement of several parameters of 5-HT presynapses allows to differentiate between treatments which exclusively affect the density of 5-HT transporters (long-term food restriction), which exclusively affect the level of tryptophan hydroxylase apoenzyme (imipramine treatment of olfactory bulbectomized rats) or which cause a parallel increase (bulbectomy, chronic administration of tranylcypramine to rats with chemical lesions of their cortical 5-HT innervation) or a parallel decrease (administration of p-chloroamphetamine) of both parameters, indicating treatment-induced changes in the density of 5-HT presynapses in the frontal cortex. Each of these changes may lead to an altered output of serotonergic afferences, and may therefore act to either potentiate or to attenuate the impact of serotonin-mediated effects on the activity of local networks located in a certain brain region.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01273313
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  • 2
    Electronic Resource
    Electronic Resource
    No evidence for a physiological coupling between melatonin and glucocorticoids (1997)
    Springer
    Psychopharmacology 133 (1997), S. 313-322 
    Details
    ISSN: 1432-2072
    Keywords: Key words Glucocorticoids ; Cortisol ; Corticosterone ; Stress ; Melatonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Much has been speculated about the existence of a physiological coupling between melatonin and glucocorticoid secretion and about a possible anti-stress action of melatonin. We examined the relationship between melatonin and glucocorticoid secretion under close-to-physiological conditions, when the plasma concentration of either melatonin or glucocorticoids was elevated acutely or chronically in both rats and humans. Tryptophan administration caused a massive rise of plasma melatonin, but had no effect on corticosterone levels in rats or on cortisol levels in humans. The acute and long-lasting exposure of rats to uncontrollable stress resulted in a significant rise of adrenal corticosterone secretion, but had no effect on circulating melatonin levels. Orchectomy caused an initial increase in circulating corticosterone (when melatonin was unaffected) and a delayed rise in circulating melatonin (when corticosterone levels were normalized). In humans, no correlation was found between the nocturnal urinary excretion of melatonin and cortisol, either among healthy subjects, or among patients suffering from panic disorder (with an increased urinary excretion of cortisol) or among insomnia patients (with a high incidence of low melatonin secretion). Furthermore, no evidence was found for a suppressive action of melatonin on dexamethasone-mediated thymus regression in rats and on dexamethasone-mediated suppression of lymphocyte proliferation in vitro. Taken together, the results of this study provide no evidence for the existence of mutual influences between melatonin and glucocorticoid secretion, nor do they support the proposed attenuation of glucocorticoid-mediated effects on target cells or tissues by melatonin under physiological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050408
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    Paper (German National Licenses)
    Fulltext
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