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  • 1
    Electronic Resource
    Electronic Resource
    Evidence that clomethiazole interacts with the macromolecular GABA A-receptor complex in the central nervous system and in the anterior pituitary gland (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 397-402 
    Details
    ISSN: 1432-1912
    Keywords: Clomethiazole ; GABAA-receptor complex ; Prolactin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Clomethiazole (CLOM) is known to be an anti-convulsant drug and has been also reported to decrease serum prolactin (PRL) in humans. Both effects may be mediated by an enhancement of gabaergic transmission. In order to determine if (CLOM) interacts with GABA metabolism and/or at the GABA receptor level, we studied its effect on PRL release and on the binding of various compounds that interact with the GABAA-benzodiazepine-receptor complex. Intraperitoneal (IP) administration of CLOM to rats significantly decreased PRL levels, and this effect was antagonized by IP administration of bicuculline, an antagonist of the GABAA receptor. In vitro, the inhibitory effect of muscimol on PRL release from rat hemiadenohypophysis was potentiated in a dose-dependent manner by preincubation with CLOM. This effect was antagonized by picrotoxin (10−6 M). On the other hand, CLOM had no effect on GABA metabolism and did not compete with GABAA, GABAB or benzodiazepine binding sites in cortical membranes. GLOM competed, however, with the picrotoxin binding site labelled with [35S]-butylbicyclophosphoro-thionate (TBPS), at an IC50 value of 1.2 × 10−4 M, which is in the same range as some barbiturates. These results concerning PRL release and binding experiments with cortical membranes suggest that GLOM interacts with the picrotoxin/barbiturate site of the GABAA-receptor-chloride channel complex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00736053
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  • 2
    Electronic Resource
    Electronic Resource
    Receptors and transduction mechanisms in anterior pituitary: Primary cultures, transfected clonal cells and human tumor derived cells (1992)
    Springer
    Cell biology and toxicology 8 (1992), S. 19-28 
    Details
    ISSN: 1573-6822
    Keywords: Adenohypophysis ; cell culture ; receptors ; transduction mechanisms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Conclusion In conclusion anterior pituitary cells represent a very good model for the study of receptors andtransduction mechanisms. Each cellular model has its limitation, heterogeneity, non-physiological regulation, and species specificity. However, combination of approaches givesinteresting information, useful to understand not only the physiological regulation of hormonesecretion, but also pathological situations. Since receptors present in the pituitary are alsolocated in other tissues, including the brain, the digestive tract, and the lymphocytes, theinformation can also be extended to many other functions. In fact, a given receptor seems tobe always associated with the same coupling mechanism in all target tissues. In contrast,receptor and G protein concentrations, coupling efficiency and cross talk betwen transductionprocesses appear specific of a given cell type. These parameters are thus likely to play animportant role in the specificity of cellular responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00130507
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Somatostatin increases mitogen-induced IL-2 secretion and proliferation of human jurkat T cells via sst3 receptor isotype (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 62-73 
    Details
    ISSN: 0730-2312
    Keywords: somatostatin ; receptor isotypes ; adenylyl cyclase ; Interleukin-2 (IL-2) ; proliferation ; Jurkat cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The neuropeptide somatostatin (SRIF) modulates normal and leukemia T cell proliferation. However, neither molecular isotypes of receptors nor mechanisms involved in these somatostatin actions have been elucidated as yet. Here we show by using RT-PCR approach that mitogen-activated leukemia T cells (Jurkat) express mRNA for a single somatostatin receptor, sst3. This mRNA is apparently translated into protein since specific somatostatin binding sites (KI1 = 78 ± 3 pM) were detected in semipurified plasma membrane preparations by using 125I-Tyr1-SRIF14 as a radioligand. Moreover, somatostatin inhibits adenylyl cyclase activity with similar efficiency (IC50 = 23 ± 4 pM) thus strongly suggesting a functional coupling of sst3 receptor to this transduction pathway. The involvement of sst3 receptor in immuno-modulatory actions of somatostatin was assessed by analysis of neuropeptide effects on IL-2 secretion and on proliferation of mitogen-activated Jurkat cells. Our data show that in the concentrations comprised between 10 pM and 10 nM, somatostatin potentiates IL-2 secretion. This effect is correlated with somatostatin-dependent increase of Jurkat cell proliferation since the EC50 concentrations for both actions were almost identical (EC50 = 22 ± 9 pM and EC50 = 12 ± 1 pM for IL-2 secretion and proliferation, respectively). Altogether, these data strongly suggest that in mitogen-activated Jurkat cells, somatostatin increases cell proliferation through the increase of IL-2 secretion via a functional sst3 receptor negatively coupled to the adenylyl cyclase pathway. J. Cell. Biochem. 68:62-73, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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    Paper (German National Licenses)
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