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  • 1
    Digitale Medien
    Digitale Medien
    Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: L-Glutamate, N-methyl-D-aspartic acid (NMDA), quisqualate, and kainate were found to increase endogenous somatostatin release from primary cultures of rat cortical neurons in a dose-dependent manner. The rank order of potency calculated from the dose-response curves was quisqualate 〉 glutamate = NMDA 〉 kainate, with EC50 values of 0.4, 20, and 40 μM, respectively. Alanine, glutamine, and glycine did not modify the release of somatostatin. The stimulation of somatostatin release elicited by L-glutamate was Ca2+ dependent, was decreased by Mg2+, and was blocked by DL-amino-5-phosphonovaleric acid (APV) and thienyl-phencyclidine (TCP), two specific antagonists of NMDA receptors. The NMDA stimulatory effect was strongly inhibited by APV in a competitive manner (IC50= 50 μM) and by TCP in a noncompetitive manner (IC50= 90 nM). The release of somatostatin induced by the excitatory amino acid agonists was not blocked by tetrodotoxin (1 μM), a result suggesting that tetrodotoxin-sensitive, sodium-dependent action potentials are not involved in the effect. Somatostatin release in response to NMDA was potentiated by glycine, but the inhibitory strychnine-sensitive glycine receptor did not appear to be involved. Our data suggest that glutamate exerts its stimulatory action on somatostatin release essentially through an NMDA receptor subtype.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07406.x
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  • 2
    Digitale Medien
    Digitale Medien
    Glutamate Peripherally Administered Exerts Somatostatin-Releasing Action in the Conscious Rat (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 3 (1991), S. 0 
    Details
    ISSN: 1365-2826
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: This study was designed to determine whether glutamate is able to stimulate somatostatin release from in vivo conscious animals when somatostatin release is monitored in unanaesthetized rats stereotaxically implanted with a push-pull cannula in the median eminence. One week after implantation, the median eminence was perfused with artificial cerebrospinal fluid alone or with the addition of either CGS 19755, an N-methyl-D-aspartate (NMDA) receptor antagonist (1(10−6 M), or glutamate (10−5 M). The latter (which is able to cross the brain-blood barrier at large doses) was also peripherally administered (1 g/kg ip). Median eminence perfusate samples were collected every 15 min and somatostatin was measured by a sensitive radioimmunoassay.In rats receiving ip glutamate injection, somatostatin release from the median eminence was significantly increased (73.3±10.4 versus 24.8 ± 6.2; P 〈 0.01; n = 5) when compared to baseline levels measured in the same animals, but no effect was observed when local perfusion of the median eminence with glutamate (10−4 to 10−5 M; n = 6) was performed. Glutamate-induced somatostatin release was completely blunted (n = 5) by prior local administration of CGS 19755 (10−5 M), a potent NMDA-type receptor antagonist able to cross the blood-brain barrier. In contrast, administration of glutamic acid diethylester, a competitive antagonist of non-NMDA receptors, at doses of 10−4 M (n = 4), was not able to alter this response.Our results are the first in vivo evidence in favour of a neuroendocrine role for glutamate on somatostatin release whose site of action seems to exclude the median eminence.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1365-2826.1991.tb00299.x
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  • 3
    Digitale Medien
    Digitale Medien
    Rapid Changes in Somatostatin and TRH mRNA in Whole Rat Hypothalamus in Response to Acute Cold Exposure (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 6 (1994), S. 0 
    Details
    ISSN: 1365-2826
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Acute cold stimulus induces activation of the thyreotropic axis characterized by a rapid increase in plasma thyrotropin (TSH). Since pituitary TSH release is mainly regulated by two hypothalamic hormones: thyrotropin-releasing hormone (TRH) and somatostatin, the aim of this study was to analyse whether changes in the steady state mRNA levels and peptide content of these neurohormones occur under acute cold stimulation in rats. Northern blot analysis of hypothalamic somatostatin mRNA levels after 15, 30, 60 or 180 min of cold exposure revealed a 2.0-fold increase after 15 min at 4°C. This augmentation was followed by a return to control values at 30 min. However, the hypothalamic content of somatostatin was not significantly modified at any cold exposure time. TRH mRNA showed a similar pattern to somatostatin, with a 2.5-fold increase after 15 min at 4°C. In contrast, hypothalamic TRH content was significantly decreased after 15 min cold exposure, returning to control values at 30 min. The increase in mRNA levels was specific for the two hypothalamic hormones, since there was no concomitant variation in GAPDH mRNA used as negative control. These results suggest that the organism is quickly aroused by cold stimulus, triggering rapid activation in transcription of the two neurohormones involved in the regulation of the thyreotrope axis. Since the peptide contents did not show the same pattern, a quantitative change in transcription or in mRNA stability does not appear to be a prerequisite for increased peptide expression, suggesting that somatostatin and TRH gene expressions could be regulated at translational or post-translational steps.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1365-2826.1994.tb00550.x
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  • 4
    Digitale Medien
    Digitale Medien
    Phospholipase A2 and Somatostatin Release are Activated in Response to N-Methyl-D-Aspartate Receptor Stimulation in Hypothalamic Neurons in Primary Culture (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 3 (1991), S. 0 
    Details
    ISSN: 1365-2826
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: We have recently shown that glutamate primarily induces somatostatin release in hypothalamic neurons through N-methyl-D-aspartate (NMDA)-type receptor sites. Here we report that glutamate and NMDA also stimulate the release of [3H]arachidonic acid in a dose-dependent manner. The NMDA-induced effects (arachidonic acid release and somatostatin secretion) were both inhibited by MK-801, an NMDA receptor-type antagonist, or mepacrine, a phospholipase A2 inhibitor. In addition, mepacrine was able to inhibit A23187-stimulated arachidonic acid release and somatostatin secretion. p-Bromophenacylbromide, another phospholipase A2 inhibitor, also blocked NMDA-induced secretion of somatostatin. However, responses to NMDA were unaffected by H7 (inhibitor of protein kinase C), nordihydroguaiaretic acid or indomethacin (inhibitors of lipoxygenase and cyclooxygenase). Melittin, a phospholipase A2 activator, was found to stimulate both responses, but omission of extracellular Ca2+ from the incubation media strongly reduced melittin-induced somatostatin release. Six-h pertussis toxin pretreatment did not significantly reduce the action of NMDA on either of the two parameters studied. High-performance liquid chromatography analysis of [3H]metabolites released in the medium after NMDA stimulation revealed that [3H]arachidonic acid was the only detectable metabolite. External addition of arachidonic acid increased the release of somatostatin, whereas E2 and F2α prostaglandins had no effect. Our results show a close correlation between arachidonic acid release and somatostatin secretion, the two parameters we investigated.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1365-2826.1991.tb00312.x
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  • 5
    Digitale Medien
    Digitale Medien
    Rapid and opposite effects of dexamethasone on in vivo and in vitro hypothalamic somatostatin release (1997)
    Springer
    Experimental brain research 113 (1997), S. 337-342 
    Details
    ISSN: 1432-1106
    Schlagwort(e): Somatostatin ; Hypothalamus ; Dexamethasone ; Picrotoxin ; Push-pull perfusion ; Rat
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract We have previously reported the rapid response of hypothalamic somatostatin (SS) neurons to acute stress. Since it is well known that glucocorticoids (GC) are involved in neuroendocrinal stress regulation, we investigate in this study the effects of acute administration of dexamethasone (Dex) on both in vivo and in vitro SS release. Freely moving animals received stereotaxic implant of a push-pull cannula into the median eminence for 10 days, and then they were perfused with artificial cerebrospinal fluid for 120–150 min. An i.p. injection of Dex (200 or 300 μg/100 g) induced, 15–30 min later, a mean increase in SS hypothalamic output of 62.6±6.2% of basal secretion. By contrast, after 15 min incubation of hypothalamic fragments with either 10−7 or 10−6 M Dex, SS release decreased abruptly to 57.3±3.3% (n=16;P〈0.001 compared with basal release) and 78.0±9.5% (n=13;P〈0.05 compared with basal release) of basal release, respectively. Other Dex concentrations induced no variations, giving the dose-effect curve an abrupt “on-off” effect. The inhibitory effect was blocked by picrotoxin (10−4 M) and was immediately reversed when Dex was removed from the medium. Specificity was tested by using another steroid, estradiol, and another tissue, cortex. The rapid action of GC whatever the model used and in particular the blocking in vitro effect of picrotoxin could suggest that GCs act at the level of the membrane and could operate physiologically in response to stress. In addition, the opposite in vivo and in vitro effects on SS release would indicate that GCs exert two different controls on SS neurons.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF02450331
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