Posted by SLS on May 13, 2009, at 6:42:01
In reply to Re: Little more, posted by linkadge on May 12, 2009, at 21:58:25
> >I am uncertain as to what are the effects on >serotoninergic neurotransmission after chronic >exposure. It is quite possible that >serotoninergic activity is enhanced rather than >suppressed.
>
> I suppose thats possible, although I havn't seen studies either way. I just personally don't think that enhancement of serotonin neurotransmission has a whole lot to do with antidepressant action. Take the most effective antidepressant (ECT), some of the most recent and comprehensive studies that ECT has not appreciable or measurable effect on serotonergic neurotransmission. I guess I am just arguing with the logic: "if it doesn't increase serotonin, it can't be an antidepressant".I am in complete agreement with you.
I think it is helpful to think of depression as a diagnosis fraught with a heterogeneity of etiologies that demand a heterogeneity of treatments. It might be that the SSRIs are the best choice for some people - regardless of how they work. As you indicate, it may still have little to do with serotonin. Still, it is becoming a more common finding that 5-HT1a receptors are subsensitive in at least some cases of major depressive disorder (MDD).
Antidepressants don't seem to work in 5-HT1a receptor knockout mice with respect to anxiety related behavior.
- Scott
poster:SLS
thread:895287
URL: http://www.dr-bob.org/babble/20090505/msgs/895507.html