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  • 1
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    Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-05-04
    Description: There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillaber, Inge -- Rammes, Gerhard -- Zimmermann, Stephan -- Mahal, Beatrice -- Zieglgansberger, Walter -- Wurst, Wolfgang -- Holsboer, Florian -- Spanagel, Rainer -- New York, N.Y. -- Science. 2002 May 3;296(5569):931-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany. sillaber@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988580" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; *Alcohol Drinking ; Alcoholism/*etiology/genetics ; Animals ; Brain/metabolism ; Corticotropin-Releasing Hormone/physiology ; Ethanol/blood ; Female ; Hippocampus/physiology ; In Vitro Techniques ; Male ; Mice ; Mice, Knockout ; Models, Animal ; Mutation ; Receptors, AMPA/metabolism ; Receptors, Corticotropin-Releasing Hormone/*genetics/*physiology ; Receptors, Kainic Acid/metabolism ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Signal Transduction ; Stress, Physiological/physiopathology ; Stress, Psychological/*physiopathology ; Up-Regulation
    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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  • 2
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    Sequence interpretation. Functional annotation of mouse genome sequences (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-03-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nadeau, J H -- Balling, R -- Barsh, G -- Beier, D -- Brown, S D -- Bucan, M -- Camper, S -- Carlson, G -- Copeland, N -- Eppig, J -- Fletcher, C -- Frankel, W N -- Ganten, D -- Goldowitz, D -- Goodnow, C -- Guenet, J L -- Hicks, G -- Hrabe de Angelis, M -- Jackson, I -- Jacob, H J -- Jenkins, N -- Johnson, D -- Justice, M -- Kay, S -- Kingsley, D -- Lehrach, H -- Magnuson, T -- Meisler, M -- Poustka, A -- Rinchik, E M -- Rossant, J -- Russell, L B -- Schimenti, J -- Shiroishi, T -- Skarnes, W C -- Soriano, P -- Stanford, W -- Takahashi, J S -- Wurst, W -- Zimmer, A -- International Mouse Mutagenesis Consortium -- New York, N.Y. -- Science. 2001 Feb 16;291(5507):1251-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, BRB 624, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106, USA. jhn4@po.cwru.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11233449" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; *Computational Biology ; Costs and Cost Analysis ; Genes/physiology ; Genetic Techniques ; *Genome ; *Genomics ; International Cooperation ; Mice/*genetics ; Mutagenesis ; Mutation ; Phenotype ; Private Sector ; Public Sector ; Research Support as Topic ; *Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Rescue of the En-1 mutant phenotype by replacement of En-1 with En-2 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-08-04
    Description: The related mouse Engrailed genes En-1 and En-2 are expressed from the one- and approximately five-somite stages, respectively, in a similar presumptive mid-hindbrain domain. However, mutations in En-1 and En-2 produce different phenotypes. En-1 mutant mice die at birth with a large mid-hindbrain deletion, whereas En-2 mutants are viable, with cerebellar defects. To determine whether these contrasting phenotypes reflect differences in temporal expression or biochemical activity of the En proteins, En-1 coding sequences were replaced with En-2 sequences by gene targeting. This rescued all En-1 mutant defects, demonstrating that the difference between En-1 and En-2 stems from their divergent expression patterns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanks, M -- Wurst, W -- Anson-Cartwright, L -- Auerbach, A B -- Joyner, A L -- New York, N.Y. -- Science. 1995 Aug 4;269(5224):679-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular and Developmental Biology, Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7624797" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/abnormalities/embryology ; Chimera ; Crosses, Genetic ; Female ; *Gene Expression Regulation, Developmental ; *Gene Targeting ; *Genes, Homeobox ; Homeodomain Proteins/*genetics/physiology ; Limb Deformities, Congenital ; Male ; Mice ; Mutation ; Nerve Tissue Proteins/*genetics/physiology ; Phenotype ; Promoter Regions, Genetic ; Recombination, Genetic ; Stem Cells ; Sternum/abnormalities
    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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  • 4
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    Glutamatergic and dopaminergic neurons mediate anxiogenic and anxiolytic effects of CRHR1 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-03
    Description: The corticotropin-releasing hormone receptor 1 (CRHR1) critically controls behavioral adaptation to stress and is causally linked to emotional disorders. Using neurochemical and genetic tools, we determined that CRHR1 is expressed in forebrain glutamatergic and gamma-aminobutyric acid-containing (GABAergic) neurons as well as in midbrain dopaminergic neurons. Via specific CRHR1 deletions in glutamatergic, GABAergic, dopaminergic, and serotonergic cells, we found that the lack of CRHR1 in forebrain glutamatergic circuits reduces anxiety and impairs neurotransmission in the amygdala and hippocampus. Selective deletion of CRHR1 in midbrain dopaminergic neurons increases anxiety-like behavior and reduces dopamine release in the prefrontal cortex. These results define a bidirectional model for the role of CRHR1 in anxiety and suggest that an imbalance between CRHR1-controlled anxiogenic glutamatergic and anxiolytic dopaminergic systems might lead to emotional disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Refojo, Damian -- Schweizer, Martin -- Kuehne, Claudia -- Ehrenberg, Stefanie -- Thoeringer, Christoph -- Vogl, Annette M -- Dedic, Nina -- Schumacher, Marion -- von Wolff, Gregor -- Avrabos, Charilaos -- Touma, Chadi -- Engblom, David -- Schutz, Gunther -- Nave, Klaus-Armin -- Eder, Matthias -- Wotjak, Carsten T -- Sillaber, Inge -- Holsboer, Florian -- Wurst, Wolfgang -- Deussing, Jan M -- New York, N.Y. -- Science. 2011 Sep 30;333(6051):1903-7. doi: 10.1126/science.1202107. Epub 2011 Sep 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21885734" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; *Anxiety ; Behavior, Animal ; Corticotropin-Releasing Hormone/metabolism ; Dopamine/*metabolism ; Fear ; Glutamic Acid/*metabolism ; Hippocampus/metabolism ; Male ; Memory ; Mesencephalon ; Mice ; Mice, Knockout ; Motor Activity ; Neurons/*metabolism ; Prefrontal Cortex/metabolism ; Prosencephalon/cytology/metabolism ; Receptors, Corticotropin-Releasing Hormone/antagonists & ; inhibitors/genetics/*metabolism ; Synaptic Transmission ; Ventral Tegmental Area/metabolism ; gamma-Aminobutyric Acid/metabolism
    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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  • 5
    Electronic Resource
    Electronic Resource
    Acute haemodynamic effects of urapidil in patients with chronic left ventricular failure (1988)
    Springer
    European journal of clinical pharmacology 35 (1988), S. 305-308 
    Details
    ISSN: 1432-1041
    Keywords: urapidil ; left ventricular failure ; haemodynamic parameters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Urapidil, a new alpha1-adrenoceptor blocking drug, has been shown to be effective in the treatment of hypertension. Ten normotensive patients with severe congestive heart failure were given Urapidil 25 mg i.v. twice in 15 min and the haemodynamic effects were measured. There was a significant fall in systolic blood pressure (−16%), mean blood pressure (−13%), left ventricular end-diastolic pressure (−38%), mean pulmonary artery pressure (−31%) and wedge pressure (−40%). Total peripheral resistance fell by 25%, whereas pulmonary arteriolar resistance did not change significantly. Cardiac output increased by 22%. The increase in cardiac output with decreasing peripheral resistance and LV pressures suggests that urapidil may be useful in the therapy of congestive heart failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00558269
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  • 6
    Electronic Resource
    Electronic Resource
    Lack of pharmacodynamic and pharmacokinetic interaction between pantoprazole and phenprocoumon in man (1996)
    Springer
    European journal of clinical pharmacology 51 (1996), S. 277-281 
    Details
    ISSN: 1432-1041
    Keywords: Key words Pantoprazole; Proton pump inhibitor drug interaction ; oral anticoagulant phenprocoumon ; pharmacodynamics ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: Pantoprazole is a selective proton pump inhibitor characterized by a low potential to interact with the cytochrome P450 enzymes in man. Due to the clinical importance of an interaction with anticoagulants, this study was carried out to investigate the possible influence of pantoprazole on the pharmacodynamics and pharmacokinetics of phenprocoumon. Methods: Sixteen healthy male subjects were given individually adjusted doses of phenprocoumon to reduce prothrombin time ratio (Quick method) to about 30–40% of normal within the first 5–9 days and to maintain this level. The individual maintenance doses remained unaltered from day 9 on and were administered until day 15. Additionally, on study days 11–15, pantoprazole 40 mg was given per once daily. As a pharmacodynamic parameter, the prothrombin time ratio was determined on days 9 and 10 (reference value) and on days 14 and 15 (test value), and the ratio test/reference was evaluated according to equivalence criteria. Results: The equivalence ratio (test/reference) for prothrombin time ratio was 1.02 (90% confidence interval 0.95–1.09), thus fulfilling predetermined bioequivalence criteria (0.70–1.43). The pharmacokinetic characteristics AUC0–24h and Cmax of S(−)-and R(+)-phenprocoumon were also investigated using equivalence criteria. Equivalence ratios and confidence limits of AUC0–24h and of Cmax of S(−)-phenprocoumon (0.93, 0.87–1.00 for AUC0–24h; 0.95, 0.88–1.03 for Cmax) and of R(+)-phenprocoumon (0.89, 0.82–0.96; 0.9, 0.83–0.98) were within the accepted range of 0.8–1.25. Conclusion: Pantoprazole does not interact with the anticoagulant phenprocoumon on a pharmacodynamic or pharmacokinetic level. Concomitant treatment was well tolerated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050198
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of urapidil on steady-state serum digoxin concentration in healthy subjects (1989)
    Springer
    European journal of clinical pharmacology 37 (1989), S. 193-194 
    Details
    ISSN: 1432-1041
    Keywords: urapidil ; digoxin ; blood drug level ; pharmacokinetics ; drug absorption/-interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In an open, randomized, two-period change-over study the effect of urapidil, an antihypertensive agent, on steady-state serum digoxin levels was investgated in 12 healthy male volunteers. The subjects were given digoxin 0.25 mg once daily for 4 days to produce a steady-state digoxin level in serum. At the end of that time the subjects received either digoxin monotherapy or digoxin and concomitant treatment with urapidil 60 mg b.d. for a further 4 days. Subsequently the treatments were changed over. The absorption characteristics Cmax and tmax of digoxin were not altered by concomitant urapidil treatment. The geometric mean and nonparametric 95% confidence limits of digoxin relative bioavailability were 97% (93%–103%). Therefore, concomitant administration of urapidil with digoxin treatments did not appear to alter the rate and extent of absorption of the glycoside.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00558231
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  • 8
    Electronic Resource
    Electronic Resource
    A novel family of repeat sequences in the mouse genome responsive to retinoic acid (1996)
    Springer
    Mammalian genome 7 (1996), S. 741-748 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Repetitive DNA sequences form a substantial portion of eukaryotic genomes and exist as members of families that differ in copy number, length, and sequence. Various functions, including chromosomal integrity, gene regulation, and gene rearrangement have been ascribed to repetitive DNA. Although there is evidence that some repetitive sequences may participate in gene regulation, little is known about how their own expression may be regulated. During the course of gene trapping experiments with embryonic stem (ES) cells, we identified a novel class of expressed repetitive sequences in the mouse, using 5′ rapid amplification of cDNA ends-polymerase chain reaction (5′ RACE-PCR) to clone fusion transcripts from these lines. The expression of these repeats was induced by retinoic acid (RA) in cultured ES cells examined by Northern blot analyses. In vivo, their expression was spatially restricted in embryos and in the adult brain as determined by RNA in situ hybridization. We designated this family of sequences as Dr (developmentally regulated) repeats. The members of the Dr family, identified by cDNA cloning and through database search, are highly similar in sequence and show peculiar structural features. Our results suggest the expression of Dr-containing transcripts may be part of an ES cell differentiation program triggered by RA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900224
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  • 9
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    Corticotropin-releasing hormone activates ERK1/2 MAPK in specific brain areas (2005)
    National Academy of Sciences
    Details
    Publication Date: 2005-04-15
    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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  • 10
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    Tumor suppressor down-regulated in renal cell carcinoma 1 (DRR1) is a stress-induced actin bundling factor that modulates synaptic efficacy and cognition (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-03
    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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