Posted by conundrum on February 22, 2010, at 22:47:28
In reply to Re: D2 And 5HT2A: Dopamine Blocking And Boosting, posted by Brainbeard on February 22, 2010, at 13:15:03
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.
This stuff is getting too confusing it seems. Is 5 HT2a attenuation of amphetamine dopaminergic release an accurate display of its actions? Usually those transporters aren't working in reverse.
Found another study showing that a 5 HT2A antagonist has antipsychotic properties but none for depression or anxiety.
http://jpet.aspetjournals.org/content/277/2/968.abstract?ref=Sawos.Org
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. See below.
http://jpet.aspetjournals.org/content/302/3/983.abstract
Then this study shows the same drug increases NE extracellular levels in the PFC.
http://dx.doi.org/10.1016/S0014-2999(00)00173-4
More confusion ensues regarding effects in other parts of the brain...hypothalmus 5 ht2a antagonist decreases NE levels here preventing hyperthermia.
http://www.ncbi.nlm.nih.gov/pubmed/11164765
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).
So apparently this just got really confusing. Fully elucidating which antagonist do what is hard to say. None of this stuff occurs in a vacuum. In the end trying to understand it may be a waste of time. Drug trials may be less nerve wracking then trying to go the scientific route, especially when you don't fully understand everything in the studies, when you don't understand how the brain regions work together, when you don't know if the data was cooked up by a drug company.
poster:conundrum
thread:907193
URL: http://www.dr-bob.org/babble/neuro/20091104/msgs/937725.html