Posted by daizy on March 5, 2003, at 7:47:36
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
Well Thanx for telling your theory, Its very interesting, you know it seems to make a lot of sense, and explains why some drugs work and others just make it worse!
>"Most researchers attribute the "wellbeing" effect of alcohol to be due to its potentiation of GABA, however there is also some increased dopamine transmission that takes place as well. The effects of GHB are two-fold. First, it increases the effectiveness of GABA for several hours, causing feelings of wellbeing and disinhibition. Over the course of these hours, it also blocks the transmission of dopamine, causing dopamine levels to build up in the brain"
Yes michael, this is true with my experience of taking GHB. I believe this is what happens when taking MDMA also, correct me if Im wrong.
>"Also, GABA is the most abundant modulator in the brain, around 30% of all transmitters. Low levels have been associated with panic attacks, anxiety disorders, insomnia and a variety of other problems"
> "DOPAMINE: I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION. Here's why: High levels of dopamine linked with paranoia, schizophrenia, stress and panic disorders, all of which have high incidences of SP. Also, in animal studies it has been shown that dopamine levels skyrocket after incidences of social defeat. THis dopamine release leads to reducing binding potential of dopamine to its receptors by decreasing number of dopamine receptors. Finnish studies have shown that people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain" Or could this also be because of, in my instance, taking drugs that then increased dopamine?
>"So basically: Low GABA = High Dopamine levels = downregulation of Dopamine receptors = reduced sensitivity of receptors = low GABA... and the cycle continues.
> So to sum it up, it seems to me that GABA dysfunction is the main reason for SP, with poor dopamine transmission due to chronically excess levels in brain as a result of low GABA"
So does this mean that to combat SP and anxiety, you need a drug that primarily increases GABA, and then adding an SSRI or SNRI to increase the levels of others?
I think I have understood!