The article you requested is
Potential Mechanisms of Action of Atypical Antipsychotic Medications in Treatment-Resistant Depression and Anxiety.
J Clin Psychiatry 2005;66(suppl 8):30-40
© Copyright 2016 Physicians Postgraduate Press, Inc.
Access to this article is available to valid users
Still can't log in? Contact the Circulation Department at 1-800-489-1001 x4 or send email
Register: If you do not have one already, register for a free account.
The serotonin (5-HT) and norepinephrine neurons have reciprocal interactions at the level of their
cell bodies and nerve terminals. As an illustration of such connections, selective serotonin reuptake
inhibitors (SSRIs) gradually enhance serotonin transmission not only in the forebrain but also in the
locus ceruleus, thereby decreasing norepinephrine neuronal firing. In contrast, blocking 5-HT2A receptors
in the presence of serotonin reuptake inhibition using the experimental compound YM992 enhances
both serotonin and norepinephrine release. The latter pharmacologic effect may be a main contributor
to the robust antidepressant effect of adding atypical antipsychotics in SSRI-resistant patients.
In obsessive-compulsive disorder, risperidone has consistently been reported to be an effective augmentation
strategy in SSRI-resistant patients. This effect may result in part from its antagonistic
actions on dopaminergic receptors and α2-adrenoceptors on serotonin terminals.