| Literature DB >> 19541954 |
Rainer Rupprecht1, Gerhard Rammes, Daniela Eser, Thomas C Baghai, Cornelius Schüle, Caroline Nothdurfter, Thomas Troxler, Conrad Gentsch, Hans O Kalkman, Frederique Chaperon, Veska Uzunov, Kevin H McAllister, Valerie Bertaina-Anglade, Christophe Drieu La Rochelle, Dietrich Tuerck, Annette Floesser, Beate Kiese, Michael Schumacher, Rainer Landgraf, Florian Holsboer, Klaus Kucher.
Abstract
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.Entities:
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Year: 2009 PMID: 19541954 DOI: 10.1126/science.1175055
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728