ALBERT — All Library Books, journals and Electronic Records Telegrafenberg

Hits per page

hits 1 - 3 | 3 hits

Sorting

Unknown

Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors (2002)

I. Sillaber ; G. Rammes ; S. Zimmermann ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 296(5569): 931-3. doi: 10.1126/science.1069836.

add to mindlist on the mindlist

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)

Permalink

	Location	Call Number	Expected	Availability

Others were also interested in ...

PAPER CURRENT

S·F·X

Fulltext

Unknown

Translocator protein (18 kD) as target for anxiolytics without benzodiazepine-like side effects (2009)

R. Rupprecht ; G. Rammes ; D. Eser ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 325(5939): 490-3. doi: 10.1126/science.1175055.

add to mindlist on the mindlist

Details

Publication Date: 2009-06-23

Description: Most antianxiety drugs (anxiolytics) work by modulating neurotransmitters in the brain. Benzodiazepines are fast and effective anxiolytic drugs; however, their long-term use is limited by the development of tolerance and withdrawal symptoms. Ligands of the translocator protein [18 kilodaltons (kD)] may promote the synthesis of endogenous neurosteroids, which also exert anxiolytic effects in animal models. Here, we found that the translocator protein (18 kD) ligand XBD173 enhanced gamma-aminobutyric acid-mediated neurotransmission and counteracted induced panic attacks in rodents in the absence of sedation and tolerance development. XBD173 also exerted antipanic activity in humans and, in contrast to benzodiazepines, did not cause sedation or withdrawal symptoms. Thus, translocator protein (18 kD) ligands are promising candidates for fast-acting anxiolytic drugs with less severe side effects than benzodiazepines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rupprecht, Rainer -- Rammes, Gerhard -- Eser, Daniela -- Baghai, Thomas C -- Schule, Cornelius -- Nothdurfter, Caroline -- Troxler, Thomas -- Gentsch, Conrad -- Kalkman, Hans O -- Chaperon, Frederique -- Uzunov, Veska -- McAllister, Kevin H -- Bertaina-Anglade, Valerie -- La Rochelle, Christophe Drieu -- Tuerck, Dietrich -- Floesser, Annette -- Kiese, Beate -- Schumacher, Michael -- Landgraf, Rainer -- Holsboer, Florian -- Kucher, Klaus -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):490-3. doi: 10.1126/science.1175055. Epub 2009 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstrasse 7, Munich 80336, Germany. rainer.rupprecht@med.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19541954" target="_blank"〉PubMed〈/a〉

Keywords: Adult ; Alprazolam/pharmacology ; Animals ; Anti-Anxiety Agents/adverse effects/*metabolism ; Benzodiazepines/adverse effects ; Cell Line ; Drug Tolerance ; Humans ; Isoquinolines/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Neurotransmitter Agents/metabolism ; Panic Disorder/drug therapy ; Purines/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA/*metabolism ; Receptors, GABA-A/metabolism ; Substance Withdrawal Syndrome/prevention & control ; Tetragastrin ; 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