Posted by Brainbeard on February 23, 2010, at 9:07:11
In reply to Re: D2 And 5HT2A: Dopamine Blocking And Boosting » Brainbeard, posted by conundrum on February 22, 2010, at 22:47:28
> This could also explain why prozac increases DA in the cortex but not in the NAc, if the Lilly study I posted is accurate and fluoxetine is a 5 ht2a antagonist.
Yeah, but don't forget Prozac is a more potent 5HT2C-antagonist.
> This stuff is getting too confusing it seems.My idea too.
> However, another study shows that chronic treatment with an experimental SRI with 2A antagonistic properties prevents the decrease in NE normally associated with SRI use.Yes, I've seen a study showing the same for Risperdal augmentation of SSRI treatment.
> Add to this mess that I've heard that 5HT2A/C receptors don't downregulate like other receptors and only down regulate when antagonized. (don't know if thats true or not).
No, 5HT2A/C receptors downregulate throught the SSRI's indirect agonism also. It's strange, downregulation of 5HT2C-receptors at least would mediate enhanced dopaminergic functioning, as well as weight gain, but with SSRI's our picture isn't exactly one of enhanced dopaminergic functioning, althoug the weight gain does show up usually to be sure. Personally, SSRI's stimulate pleasure seeking behavior in me and tend to make me hypersexual MENTALLY, which may be symptoms of 5HT2C downregulation.
> So apparently this just got really confusing.Right.
>None of this stuff occurs in a vacuum. In the end trying to understand it may be a waste of time.
So true.
>Drug trials may be less nerve wracking then trying to go the scientific route (.....)Yeah, and how about combining hypotheses based on science with thorough experimentation? That's what I try to do, though not all of my doctors appreciate it as much.. ;)
poster:Brainbeard
thread:907193
URL: http://www.dr-bob.org/babble/neuro/20100223/msgs/937741.html