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  • 1
    Electronic Resource
    Electronic Resource
    Agmatine recognizes α2-adrenoceptor binding sites but neither activates nor inhibits α2-adrenoceptors (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1994), S. 10-16 
    Details
    ISSN: 1432-1912
    Keywords: Key words Agmatine ; α2-Adrenoceptor binding sites ; α2-Adrenoceptors ; Clonidine-displacing substance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been suggested that agmatine (decarboxylated arginine) is an endogenous clonidine-displacing substance (CDS) which recognizes α2-adrenoceptor and non-adrenoceptor, imidazoline binding sites. We have examined the effect of agmatine at α2-adrenoceptor binding sites and pre- and postjunctional α2-adrenoceptors. Agmatine produced a concentration-dependent inhibition of 1 nmol/l 3H-clonidine binding to both rat (pKi–5.10±0.05) and bovine (pKi–4.77±0.38) cerebral cortex membranes. However, agmatine (0.1–100 μM) failed to activate pre-junctional α2-adrenoceptors regulating transmitter release in the guinea-pig isolated ileum and rat isolated vas deferens, nor did it activate postjunctional α2-adrenoceptors of the porcine isolated palmar lateral vein which mediate contraction or inhibition of forskolin-stimulated cyclic AMP formation. High concentrations of agmatine (10–30-fold the pKi at α2-adrenoceptor binding sites) failed to influence α2-adrenoceptor activation by either clonidine or UK-14304 (5-bromo-6-[2-imidazolin-2-ylamino]-quinoxaline bitartrate) in any of the peripheral preparations examined. Moreover, even in a preparation where an interaction with α2-adrenoceptor binding sites on cell membranes can be demonstrated, the rat cerebral cortex, agmatine failed to inhibit forskolin-stimulated cyclic AMP in the intact tissue or affect the inhibition produced by the selective α2-adrenoceptor agonist UK-14304. Agmatine was also devoid of agonist activity in two preparations, the rat isolated thoracic aorta and the rat isolated gastric fundus, in which CDS has been reported to produce non-adrenoceptor effects. Thus, we have confirmed that agmatine recognizes α2-adrenoceptor binding sites and, therefore, is a CDS. However, since agmatine is devoid of pharmacological activity at either peripheral or central α2-adrenoceptors it can not account for earlier reports suggesting that brain-derived CDS can activate α2-adrenoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169058
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Microstimulation of movements from cerebellar-receiving, but not pallidal-receiving areas of the macaque thalamus under ketamine anaesthesia (1998)
    Springer
    Experimental brain research 123 (1998), S. 387-396 
    Details
    ISSN: 1432-1106
    Keywords: Key words Thalamus ; Basal ganglia ; Cerebellum ; Electrical stimulation ; Movement
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The motor thalamic areas receiving input from the globus pallidus (VA) and the cerebellar nuclei (VL) appear to have different roles in the generation and guidance of movements. In order to further test these differences, we used electrical stimulation to map the ventro-anterior and ventro-lateral nuclei of the thalamus in three ketamine anaesthetised monkeys. Movements were readily evoked from VL at currents of down to 10 μA. The movements were typically multi-joint, and stimulation could evoke arm and trunk or arm and facial movement at the same current threshold. Evoked arm movements often involved multiple joints, with or without finger movements. Facial movements included the lips, tongue, jaw, eyebrows and, occasionally, the eyes. The thalamic map was topographic, but complex with at least two separate regions related to arm movement. Very few sites within the VA could stimulate movement, even at high currents. We therefore suggest that the cerebellar projections to motor regions of the cortex, which pass through the VL thalamic nuclei, have a different relationship and are closer to movement execution than the projections from basal ganglia via the ventro-anterior nucleus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002210050584
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Agmatine recognizes α2-adrenoceptor binding sites but neither activates nor inhibits α2-adrenoceptors (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 10-16 
    Details
    ISSN: 1432-1912
    Keywords: Agmatine ; α2-Adrenoceptor binding sites ; α2-Adrenoceptors ; Clonidine-displacing substance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been suggested that agmatine (decarboxylated arginine) is an endogenous clonidine-displacing substance (CDS) which recognizes α2-adrenoceptor and non-adrenoceptor, imidazoline binding sites. We have examined the effect of agmatine at α2-adrenoceptor binding sites and pre- and postjunctional α2-adrenoceptors. Agmatine produced a concentration-dependent inhibition of 1 nmol/l 3H-clonidine binding to both rat (pKi–5.10+-0.05) and bovine (pKi–4.77+-0.38) cerebral cortex membranes. However, agmatine (0.1–100 μM) failed to activate pre-junctional α2-adrenoceptors regulating transmitter release in the guinea-pig isolated ileum and rat isolated vas deferens, nor did it activate post-junctional α2-adrenoceptors of the porcine isolated palmar lateral vein which mediate contraction or inhibition of forskolin-stimulated cyclic AMP formation. High concentrations of agmatine (10–30-fold the pKi at α2-adrenoceptor binding sites) failed to influence α2-adrenoceptor activation by either clonidine or UK-14304 (5-bromo-6-[2-imidazolin-2-ylamino]-quinoxaline bitartrate) in any of the peripheral preparations examined. Moreover, even in a preparation where an interaction with α2-adrenoceptor binding sites on cell membranes can be demonstrated, the rat cerebral cortex, agmatine failed to inhibit forskolin-stimulated cyclic AMP in the intact tissue or affect the inhibition produced by the selective α2-adrenoceptor agonist UK-14304. Agmatine was also devoid of agonist activity in two preparations, the rat isolated thoracic aorta and the rat isolated gastric fundus, in which CDS has been reported to produce non-adrenoceptor effects. Thus, we have confirmed that agmatine recognizes α2-adrenoceptor binding sites and, therefore, is a CDS. However, since agmatine is devoid of pharmacological activity at either peripheral or central α2-adrenoceptors it can not account for earlier reports suggesting that brain-derived CDS can activate α2-adrenoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169058
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Tumour steroid hormone synthesis and estrogen receptor status in breast cancer patients (1981)
    Springer
    Breast cancer research and treatment 1 (1981), S. 263-266 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; estrogen receptors ; steroid biosynthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The capacity of breast cancer to synthesise active androgens and estrogens has been related to estrogen receptor (ER) status in 79 postmenopausal patients with breast cancer. Although there was no quantitative relationship between levels of ER and steroid metabolism in ER positive tumours, there was (a) a positive correlation between estrogen synthesis and ER positivity and (b) increased androgen synthesis and ER negativity. This may imply an inherent difference in the handling of hormones in ER positive and negative tumours.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01806266
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Effects of drugs associated with hyperprolactinemia on plasma steroids and on steroid receptors and metabolism in human breast cancer (1983)
    Springer
    Breast cancer research and treatment 3 (1983), S. 331-338 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; estrogen receptor ; hyperprolactinemic drugs ; prolactin ; steroid biosynthesis ; steroid hormones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Certain commonly taken pharmaceutical preparations induce increased levels of plasma prolactin. The effects of these drugs on (a) tumor steroid receptors and metabolism, and (b) plasma hormones and hormone binding proteins have been studied in postmenopausal women with breast cancer. Two groups have been compared, 18 patients on drug treatment for at least 2 months and 15 subjects with no history of drug ingestion. Patients taking medication had significantly higher levels of plasma prolactin compared with control women. No significant difference was observed between the groups with regard to the plasma concentrations of dehydroepiandrosterone (DHA) and its sulphate (DHS), testosterone, estrone, estradiol-17β, sex hormone binding globulin (SHBG), and albumin. Similarly, no difference was observed between these two groups with regard to estrogen receptor (ER), progestogen receptor (PR), or androgen receptor (AR) levels in the tumors nor their ability to metabolize (7−3H) testosterone. It is considered that the ingestion of these drugs does not affect tumor mechanisms involving steroids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01807585
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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