Posted by linkadge on December 29, 2005, at 16:51:02
In reply to Why Atpyical AntiPsychotics work in TRD, posted by jrbecker on December 29, 2005, at 16:09:47
Interesting, report. I agree with much of what was said.
In his discription of the augmentative antidepressant effects of 5-ht2a antagonists in depressive disorders, I can't help but think of the TCA's, many of which have this property, in addition to monoamine uptake inhibition.
I still disagree to the use of atypical antipsychotics for this purpose. There are better ways to achieve 5-ht2a antagonism without messing around with your dopamine receptors. For SSRI augmentation, I would look at mirtazapine, trazodone, or TCA augmentation before ever resorting to an atypical. Taking an atypical is a mixed bag, the dopamine antagonism is going to be detremental.
I also don't really agree with his dismissal of the neurotrophic theory of antidepressants. Not all people worsen after amino acid depletion, but blocking the neurotrophic effects of an antidepressant is a surefire way to abolish its effect in mice. As well, tianeptine works without increasing serotonergic neurotransmission, so people are unlikely to relapse on this one after acute tryptophan depletion, (I could be wrong)
I think that an additional role of 5-ht2a antagonists in psychiatry is relavant to their ability to prevent stress induced downregulation of hippocampal neurotrophins.
http://www.jneurosci.org/cgi/content/abstract/17/8/2785
Linkadge
poster:linkadge
thread:593147
URL: http://www.dr-bob.org/babble/20051221/msgs/593165.html