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  • 1
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    Reversal of pathological pain through specific spinal GABAA receptor subtypes (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-01-19
    Description: Inflammatory diseases and neuropathic insults are frequently accompanied by severe and debilitating pain, which can become chronic and often unresponsive to conventional analgesic treatment. A loss of synaptic inhibition in the spinal dorsal horn is considered to contribute significantly to this pain pathology. Facilitation of spinal gamma-aminobutyric acid (GABA)ergic neurotransmission through modulation of GABA(A) receptors should be able to compensate for this loss. With the use of GABA(A)-receptor point-mutated knock-in mice in which specific GABA(A) receptor subtypes have been selectively rendered insensitive to benzodiazepine-site ligands, we show here that pronounced analgesia can be achieved by specifically targeting spinal GABA(A) receptors containing the alpha2 and/or alpha3 subunits. We show that their selective activation by the non-sedative ('alpha1-sparing') benzodiazepine-site ligand L-838,417 (ref. 13) is highly effective against inflammatory and neuropathic pain yet devoid of unwanted sedation, motor impairment and tolerance development. L-838,417 not only diminished the nociceptive input to the brain but also reduced the activity of brain areas related to the associative-emotional components of pain, as shown by functional magnetic resonance imaging in rats. These results provide a rational basis for the development of subtype-selective GABAergic drugs for the treatment of chronic pain, which is often refractory to classical analgesics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knabl, Julia -- Witschi, Robert -- Hosl, Katharina -- Reinold, Heiko -- Zeilhofer, Ulrike B -- Ahmadi, Seifollah -- Brockhaus, Johannes -- Sergejeva, Marina -- Hess, Andreas -- Brune, Kay -- Fritschy, Jean-Marc -- Rudolph, Uwe -- Mohler, Hanns -- Zeilhofer, Hanns Ulrich -- England -- Nature. 2008 Jan 17;451(7176):330-4. doi: 10.1038/nature06493.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nurnberg, D-91054 Erlangen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202657" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/administration & dosage/metabolism/pharmacology/therapeutic use ; Animals ; Brain/drug effects/physiology ; Capsaicin/pharmacology ; Chronic Disease/drug therapy ; Diazepam/administration & dosage/metabolism/pharmacology ; Disease Models, Animal ; Fluorobenzenes/metabolism/pharmacology ; Formaldehyde ; Ganglia, Spinal/cytology/metabolism ; Hot Temperature ; Inflammation/chemically induced/drug therapy ; Male ; Mice ; Neurons/drug effects/metabolism ; Organ Specificity ; Pain/chemically induced/*drug therapy/*metabolism/prevention & control ; Protein Isoforms/chemistry/metabolism ; Protein Subunits/chemistry/metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/chemistry/genetics/*metabolism ; Spinal Cord/cytology/drug effects/*metabolism/physiopathology ; Triazoles/metabolism/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    GlyR alpha3: an essential target for spinal PGE2-mediated inflammatory pain sensitization (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-05-08
    Description: Prostaglandin E2 (PGE2) is a crucial mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR alpha3) by PGE2-induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR alpha3 is distinctly expressed in superficial layers of the spinal cord dorsal horn. Mice deficient in GlyR alpha3 not only lack the inhibition of glycinergic neurotransmission by PGE2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal PGE2 injection or peripheral inflammation. Thus, GlyR alpha3 may provide a previously unrecognized molecular target in pain therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harvey, Robert J -- Depner, Ulrike B -- Wassle, Heinz -- Ahmadi, Seifollah -- Heindl, Cornelia -- Reinold, Heiko -- Smart, Trevor G -- Harvey, Kirsten -- Schutz, Burkhard -- Abo-Salem, Osama M -- Zimmer, Andreas -- Poisbeau, Pierrick -- Welzl, Hans -- Wolfer, David P -- Betz, Heinrich -- Zeilhofer, Hanns Ulrich -- Muller, Ulrike -- New York, N.Y. -- Science. 2004 May 7;304(5672):884-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, The School of Pharmacy, London WC1N 1AX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15131310" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Dinoprostone/administration & dosage/*metabolism/pharmacology ; Female ; Freund's Adjuvant ; Glycine/metabolism ; Humans ; Inflammation/metabolism/*physiopathology ; Male ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Neurons/metabolism ; Pain/*physiopathology ; Patch-Clamp Techniques ; Phosphorylation ; Posterior Horn Cells/*metabolism ; Receptors, Glycine/chemistry/genetics/*metabolism ; Signal Transduction ; Spinal Cord/*metabolism ; Synaptic Transmission ; Transfection ; Zymosan
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Variable sensitivity to noxious heat is mediated by differential expression of the CGRP gene (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-08-23
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Serum concentration and urinary excretion of 3H-Ouabain in patients suffering from liver or kidney diseases (1969)
    Springer
    Details
    Publication Date: 1969-03-01
    Print ISSN: 0031-6970
    Electronic ISSN: 1432-1041
    Topics: Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 5
    Electronic Resource
    Electronic Resource
    Serum concentration and urinary excretion of 3H-Ouabain in patients suffering from liver or kidney diseases (1969)
    Springer
    European journal of clinical pharmacology 1 (1969), S. 114-118 
    Details
    ISSN: 1432-1041
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Description / Table of Contents: Zusammenfassung 3H-g-Strophanthin wurde Patienten folgender drei Kategorien i.v. verabreicht: a) Kontrollpatienten b) Patienten mit eingeschränkter Leberfunktion (Cirrhose, Verschlußikterus) c) Patienten mit eingeschrankter Nierenfunktion (Pyelonephritis, Glomerulonephritis).. Bei den Kontrollpatienten nahm der Serumspiegel mit zwei Zeitkonstanten ab (t 1/2 20 min bzw. etwa 50 Std). 5–6 Std nach der Injektion betrug die Serumkonzentration nur noch 10% des Ausgangswertes. Nach 48 Std waxen etwa 61% der verabreichten Dosis mit dem Urin ausgeschieden worden. 3H-g-Strophanthin wurde in unveranderter Form eliminiert. Bei Leberkranken mit eingeschrankter Galleproduktion zeigte der zeitliche Verlauf des Serumspiegels und die Urinausscheidung dasselbe Verhalten wie bei den Kontrollpatienten. Von den nierenerkrankten Patienten dagegen worden in 48 Std nur 28% des verabreichten 3H-g-Strophanthin mit dem Urin ausgeschieden. Die Serumradioaktivität lag 6–48 Std nach der Injektion des Glykosids 2–3 mal so hoch wie bei den Kontrollen.
    Notes: Summary 3H-ouabain was administered intravenously to control patients, and to patients suffering from liver disease or renal failure. In the control patients the 3H-ouabain disappeared from the serum by two exponentials, with half-lives of about 20 min and 50 h, respectively. After 5–6 h only 8% of the initial serum concentration remained. During 48 h following drug administration about 61 % of the administered dose was excreted in the urine. 3H-ouabain was excreted as such and not metabolized. Liver disease accompanied by pathological impairment of bile production neither affected the disappearance from the serum nor the urinary excretion. During renal failure, however, only 28% of the administered 3H-ouabain was excreted with the urine during 48h. The serum level was 2–3 times higher than in the control patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404656
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  • 6
    Electronic Resource
    Electronic Resource
    Arrow's impossibility theorem (1978)
    Springer
    De economist 126 (1978), S. 84-115 
    Details
    ISSN: 1572-9982
    Source: Springer Online Journal Archives 1860-2000
    Topics: Economics
    Notes: Summary It is the purpose of this article to give an exact formulation of Arrow's famous impossibility theorem and its proof. Although the results presented here are not new in the sense that the theorem is refuted or questionned, it may be of some interest especially for the reader who wants to get a more or less complete view of the argumentation leading up to the theorem. Special attention is paid to the logical structure of the argument in the conviction that a lot of misunderstanding exists about what Arrow and subsequent writers tried to say. By way of introduction to the central theme some remarks are made concerning the relation of the Arrow problem to welfare economics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01718079
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