Posted by linkadge on January 22, 2010, at 17:54:15
In reply to Re: Surplus of SSRI receptors may lead to TRD, posted by bleauberry on January 21, 2010, at 18:07:41
I personally don't think it really explains things all that well.
For starters all sorts of studies have tried to link the expression of presynaptic 5-ht1a receptors to depression, anxiety, suicide etc.
Essentially, they have found nothing however. In some animal models, hypoactive 5-ht1a autoreceptors is linked to increased anxiety since this increases serotonergic neurotransmission in the dorsal raphai. Studies have found overexpressed and underexpressed presynaptic 5-ht1a receptor expression in human depression, suicide and anxiety.
The other thing too is that long term SSRI administration was supposed to desensitize presynaptic 5-ht1a autoreceptors. This was suggested with animal models using fluoxetine at least. So this would (in theory) counteract the overexpression of 5-ht1a autoreceptors seen in depression.
The other thing too is that running (long term) has documented antidepressant effects and it is associated with an increase in presynaptic 5-ht1a autoreceptor expression. Mind you it decreases 5-ht1b autoreceptors. So it decreases serotoninergic functioning in certain areas of the brain and increases it in others (as 5-ht1a and 5-ht1b autorceptors influence other areas of the brain).
Lithium works as a 5-ht1b autoreceptor antagonist yet it has no effect on 5-ht1a autoreceptors. Clomipramine also desensitizes 5-ht1b autoreceptors but not 5-ht1a. rTMS induces a subsensitivity of both 5-ht1a and 5-ht1b autoreceptors.
Linkadge
poster:linkadge
thread:934392
URL: http://www.dr-bob.org/babble/20100122/msgs/934702.html