Posted by SLS on September 14, 2021, at 21:11:05
In reply to Re: Why do meds constantly stop working for me?, posted by rose45 on September 14, 2021, at 17:32:09
> All the links to sulpride that I have found mention its augmentation use for schizophrenia. Not one article for its use in augmentation of anti depressants, or maois in particular.
Darn. I meant amisulpride as opposed to sulpiride. Sorry.
They are similar in that they are both selective for dopamine presynaptic autoreceptors. Those are the receptors on the first neuron at the synapse. When they "see" too much dopamine, they turn off the manufacture and release of dopamine. So, when an antagonist makes the first neuron "blind" to the excess dopamine, it continues to release it anyway. These presynaptic autoreceptors are "stickier" (higher binding affinity) than are the postsynaptic receptors on the second neuron. At low dosages, the presynaptic binding predominates, so dopamine release is increased without the postsynaptic receptors being antagonized (blocked). The postsynaptic neuron can still see dopamine and can be stimulated by it.
Anyway, like I said, amisulpride was of great interest on Psycho-Babble perhaps 20 years ago. I think there are several papers on amisulpride being a good treatment for dysthymia. Zyprexa is an entirely different beast, and I don't know how it augments MAOIs pharmacologically. 5-HT2a/c antagonism maybe? I'm sure someone will know. Zyprexa is what's called an inverse-agonist at those receptors. Basically, this means that it actually suppresses activity even more that a pure antagonist does. It's sort of like a super-antagonist.
- ScottSome see things as they are and ask why.
I dream of things that never were and ask why not.The only thing necessary for the triumph of evil is that good men do nothing.
poster:SLS
thread:1116886
URL: http://www.dr-bob.org/babble/20210723/msgs/1116945.html