RSS-Feed abonnieren
DOI: 10.1055/s-2005-866812
© Georg Thieme Verlag Stuttgart · New York
Angststörungen - Trends in der psychopharmakologischen Behandlung
Trends in the psychopharmacological treatment of anxiety disordersPublikationsverlauf
Publikationsdatum:
24. März 2005 (online)
![](https://www.thieme-connect.de/media/psychoneuro/200503/lookinside/thumbnails/10.1055-s-2005-866812-1.jpg)
Zusammenfassung
Rationalen und Ziele für die Entwicklung neuer Psychopharmaka in der Behandlung von Angststörungen sind neben einer guten Wirksamkeit ein rascher Wirkungsbeginn, gute Verträglichkeit und ausbleibende Toleranz- und Absetzeffekte. Zeitgemäße Entwicklungen zeigen Trends in der Entwicklung selektiver wirksamer serotonerger Substanzen und GABA-Modulatoren, die keine den Benzodiazepinen vergleichbaren unerwünschten Effekte zeigen. Besonders vielversprechende Ansätze zeigen Neuropeptidliganden, die in bestimmte Prozesse bei Angststörungen eingreifen. Hierzu rechnet man im Besonderen Liganden für CCK-4, Substanz-P, Neuropeptid-Y und Sigma-Rezeptoren. Ein wesentlicher zukünftiger Stellenwert ist von Substanzen zu erwarten, die Prozesse im Rahmen der neuroendokrinologischen Stressregulation modulieren, wie CRH-Rezeptorantagonisten und ANP-Agonisten. Viele dieser Strategien sind allerdings noch in frühen Phasen der klinischen Prüfung.
Summary
The rationale for, and the aims of, the development of new psychopharmacological substances for the treatment of anxiety disorders are, in addition to effectiveness, a rapid onset of effect, good tolerability and an absence of tolerance and discontinuation effects. Modern developments reveal trends in the development of selectively effective serotonergic substances and GABA modulators, which show none of the undesired effects comparable with those seen with benzodiazepines. Particularly promising approaches are the neuropeptide ligands that interfere with certain processes in anxiety disorders. These substances include in particular ligands for CCK-4, substance P, neuropeptide Y, and sigma receptors. A major future impact is to be expected from substances that modulate processes within the framework of neuroendocrinal stress regulation, such as CRH receptor antagonists and ANP agonists. It must be noted, however, that many of these strategies are still in the early stages of clinical testing.
Key Words
therapeutic interventions - anxiety - panic disorders - new strategies
Literatur
- 1 Bandelow B. et al. . WFSBP Task force on treatment guidelines for the pharmacological treatment of anxiety - obsessive compulsive disorders and posttraumatic stress disorder. World J Biol Psychiatry. 2002; 3 171-199
- 2 Deren-Wesolek A, Tatarczynska E, Chojnacka-Wojcik E. The novel buspirone analogue, 8-(4-(2-(1,2,3,4-tetrahydroisoquinolinyl)(butyl)-8-azaspiro (4.5) decane-7,9-dione, with anxiolytic-like and antidepressant-like effects in rats. J Psychopharmacol. 1998; 12 380-384
- 3 Healy DG. et al. . Metyrapone displays antidepressant-like properties in preclinical paradigms. Psychopharmacology. 1999; 145 303-308
- 4 Holsboer F. The rationale for corticotropin-releasing hormone receptor (CRH-R) antagonists to treat depression and anxiety. J Psychiatr Res. 1999; 33 181-214
- 5 Keck ME, Holsboer F. Hyperactivity of CRH neuronal circuits as a target for therapeutic interventions in affective disorders. Peptides. 2001; 22 835-844
- 6 Keck ME. et al. . The high-affinity non-peptide CRH1 receptor antagonist R121919 attenuates stress-induced alterations in plasma oxytocin, prolactin, and testosterone secretion in rats. Pharmacopsychiatry. 2003; 36 27-31
- 7 Kramer MS. et al. . Distinct mechanism for antidepressant activity by blockade of central substance P receptors. Science. 1998; 281 1640-1645
- 8 Liebsch F. et al. . Differential behavioural effects of chronic infusion of CRH1 and CRH2 receptor antisense oligonucleotides into the rat brain. J Psychiatry Res. 1999; 33 153-163
- 9 Murphy BE, Filipini D, Ghadirian AM. Possible use of glucocorticoid receptor antagonists in the treatment of major depression: preliminary results using RU 486. J Psychiatry Neurosci. 1993; 18 209-213
- 10 Nutt DJ. et al. . Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders. Eur Neuropsychopharmacol. 1999; 9 81-86
- 11 O'Dwyer AM. et al. . Teatment of amjor depression with metyrapone and hydrocortisone. J Affect Disord. 1995; 33 123-128
- 12 Pande AC. et al. . Placebo-controlled of gabapentin treatment of panic disorder. J Clin Psychopharmacol. 2000; 20 467-471
- 13 Pecknold JC. et al. . Gepirone and the treatment of panic disorder: an open study. J Clin Psychopharmacol. 1993; 13 145-149
- 14 Pelletier G, Steinbusch HW, Verhofstad AA. Immunoreactive substance P and serotonin present in the same dense-core vesicles. Nature. 1981; 293 71-72
- 15 Sandford JJ. et al. . Crossover trial of pagoclone and placebo in patients with DSM-IV panic disorder. J Psychopharmacol. 2001; 15 205-208
- 16 Sargent PA. et al. . Brain serotonin1A receptor binding measured by positron emission tomography with (11C)WAY-100635: effects of depression and antidepressant treatment. Arch Gen Psychiatry. 2000; 57 174-180
- 17 Ströhle A. et al. . Central and peripheral administration of atriopeptin is anxiolytic in rats. Neuroendocrinology. 1997; 65 210-215
- 18 Ströhle A. et al. . Anxiolytic activity of atrial natriuretic peptide in patients with panic disorder. Am J Psychiatry. 2001; 158 1514
- 19 Van Megen HJ. et al. . The cholecystokinin-B receptor antagonist CI-988 failed to affect CCK-4 induced symptoms in panic disorder patients. Psychopharmacology. 1997; 129 243-248
- 20 Van Vliet IM, Westenberg HG, Den Boer JA. Effects of the 5HT1A receptor agonist flesonoxan in panic disorder. Psychopharmacology. 1996; 127 174-180
- 21 Wedekind D, Bandelow B. Die Alpha-2-Delta-Untereinheit des spannungsabhängigen Kalziumkanals als pharmakologisches Ziel in der Psychiatrie und Neurologie. Nervenarzt (eingereicht)
- 22 Wolkowitz OM. et al. . Antiglucocorticoid treatment of depression: double-blind ketokonazole. Biol Psychiatry. 1999; 45 1070-1074
Korrespondenzadresse:
Dr. med. Dirk WedekindMSc
Klinik für Psychiarie und Psychotherapie der Georg-August-Universität Göttingen
Von-Siebold-Straße 5
37075 Göttingen
eMail: dwedeki1@gwdg.de