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Re: to Scott - Mirapex and amisulpiride

Posted by Scott L. Schofield on December 30, 1999, at 7:42:25

In reply to Re: to Scott, posted by andrewb on December 29, 1999, at 12:01:19

> I have recently had what seems like a partial poop out on amisulpride after 4 months of effectiveness. That is less energy, more daytime sleepiness and less motivation. Another person wrote that she experienced poop out after an initial robust response to Mirapex. It occurs to me that maybe we aren't experiencing poop out after all, rather I may be taking too much amisulpride and she too little Mirapex. I am taking 100 mgs/day of amisulpride though studies have shown 50 mgs./day to be just as effective. Any ideas here. What would happen if a dopamine agonist like Mirapex was combined with Amisulpride. Could this possibly be an more effective antidepressant cocktail. I also was wondering what the difference was between ropinirole and pramipexole. Perhaps the only difference is the relative degree of binding affinity to the D2 (and D3?) receptors but to the patient pretty much the same effect is experienced.

I wish I hadn’t been forced to drop out of college as a sophomore because of this damned thing. I would have had a better perspective and greater confidence in what I *think* I know. I do know that some drugs display a “therapeutic window”. A therapeutic window represents the range of dosages (or blood-levels, etc.) within which a drug will be effective. The word “window” is used to convey the idea that there is a minimum dosage and a maximum dosage within which the drug will exert its therapeutic effect. This therapeutic effect is lost if the dosage is too low or too high.

As far as amisulpiride is concerned, I think that there may be a better chance of it having a stable therapeutic window as compared to pramipexole. Your guess may be right and you could be taking too much. Low dosages of other neuroleptics have been used with varying degrees of success as antidepressants. One of the more promising drugs for this usage is olanzapine (Zyprexa).

The augmentation of antidepressants using direct-acting (ligand) dopamine agonists such as bromocryptine and pergolide has been used in the past. I have read some pretty persuasive anecdotes that support this practice. I’m not so convinced that it is so effective long-term. The few people I know who have tried it (myself included) have experienced and initial improvement followed by a plateauing and then relapse. Perhaps there are properties possessed by pramipexole that foster a continued response. For now, I just don’t have that much confidence in using DA agonists. Perhaps it is the development of postsynaptic receptor subsensitivity that might require the need for higher and higher dosages until some upper-bound is reached. This would especially be likely if the presynaptic neuron were inhibited by the stimulation of its autoreceptors. I can’t remember what all of the different dopamine receptors do or where they are located, but it seems reasonable that a compound that is a specific (rather than selective) agonist of postsynaptic receptors may be less liable to end in burn-out.

I have never thought of combining a DA agonist with a DA antagonist. It is an intriguing proposition. What if one were to combine a selective presynaptic antagonist with a selective postsynaptic agonist? Interesting stuff.

Good thinking.





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