Posted by CrAzYmEd on May 23, 2010, at 17:03:03 [reposted on May 24, 2010, at 22:42:06 | original URL]
In reply to Let's Have Dopamine Pie For Lunch, posted by Brainbeard on May 23, 2010, at 16:39:49
"5HT2A receptors INHIBIT dopamine, my good friend. So AGONIZING them may boost dopamine in certain area's of the brain only by inhibiting it in other area's."
--- If i'm correct 5HT2A antagonism boosts dopamine in the same area's as 5HT1A agonism, but 5HT2A agonism increases dopamine in mesolimbic area's, thus making the combo of 5HT1A/5HT2A agonism the most interesting.
"D2 agonism can promote psychotic symptoms and weird thought patterns.'
----- Sure, in psychotic ppl it will make everything worse, HOWEVER that doesnt mean they will cause psychotic symptons if those that arent psychotic (for example look at all the studies regarding pramipexole, its generally well tolerated and has been shown VERY effective for depression.
A good friend of me with social anxiety has been on pramipexole for months for he's social anxiety,with great succes, however he did get anhedonia, wich is caused by D3 agonism (D3 preferring agonists cause gambling by blunting reward).
"D4 receptors are involved with prefrontal information processing. An experimental D4-ANTAGONIST has been shown to REDUCE stress induced cognitive debilitation.
The ' atypical typical' antipsychotic pipamperone is a potent D4-antagonist and this has been theorized to be one of the mechanisms behind its therapeutic potential for mood disorders.. together with 5HT2A-antagonism."---- Agreed, however both agonism and antagonism can have differend positive effects for many receptors.
"There is evidence to suggest that D2-antagonism combined with serotonin reuptake inhibition boosts dopamine transmission in the prefrontal cortex: http://www.nature.com/npp/journal/v30/n1/abs/1300567a.html"
----Presynaptic antagonism.
"Dopamine agonism is not what you may think it is: it fools the brain into thinking there is more dopamine around, without actually increasing dopaminergic transmission! That's why dopamine agonists can have such non-dopaminergic side-effects as causing one to fall asleep in the middle of activity (all synthetic D2-agonists can cause sleep attacks, with the noteable exception of piribedil=Trivastal)!"
-----I know, however autoreceptors up/downregulate, so with chronic administration the side effects will greatly reduce leaving you with more D2 activation, i'm aware of the autoreceptors;).
"Like most all of us, including my good self, you're oversimplifying way too much here. You're jumping from dopamine in general to D2 agonism. Risperdal is a drug that has helped many with social anxiety, often as an add-on to an SSRI. Risperdal is a 5HT2A-antagonist and a D2-antagonist."
---- While i agree that it would help anxiety, i beleive that dopamine agonism in combination with 5HT1A agonism is the way to go. Dopamine agonism in some brainarea's causes anxiety, however 5HT1A agonism fully counteracts that (as lisuride doesnt cause any increase in anxiety but is highly anxiolytic), so the benefits of D2 agonism show up.
Dopamine boosting drugs are far better for SA then risperdal SSRI, for example amphetamine is considered the most effective med for it on the SA forum i post.
Or sulpiride AMI, a friend of me has great succes with that combo, the sulpiride blocks the presynaptic's, so the prami fully agonizes the postsynaptic receptors.
poster:CrAzYmEd
thread:948688
URL: http://www.dr-bob.org/babble/neuro/20100223/msgs/948716.html