Posted by Brainbeard on May 23, 2010, at 16:39:49 [reposted on May 24, 2010, at 22:42:05 | original URL]
In reply to Re: Interesting - Could Be Key Ingredient Of AD Combo, posted by CrAzYmEd on May 23, 2010, at 16:06:54
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.
Agonism may yield results similar to antagonism through downregulation and similar mechanisms. Remember that SSRI's are only effective after weeks to months because only then the therapeutical effects of indirect 5HT2A-agonism (through flooding the brain with serotonin=5HT) become manifest. Still, 5HT2A/C-antagonism appears to be a better way to boost dopamine than ditto agonism.
D2 agonism can promote psychotic symptoms and weird thought patterns.
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.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
> Dopamine is also implicated in social anxiety, so D2 agonism would be of benefit it, and not D2 antagonism (wich i think is a bad idea overall, agonism is the way to go).
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.
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)!
Current meds: 10mg melitracene + 0.5mg flupentixol; sertraline 100mg; amitriptyline 25mg; gabapentin (Neurontin) 300mg; melatonin 0.3mg. PRN: diazepam (Valium) 2.5-5mg.
poster:Brainbeard
thread:948688
URL: http://www.dr-bob.org/babble/neuro/20100223/msgs/948715.html