Kenaz
Bluelighter
After writing a book on poppies, I'm working on a book on the history of melancholia. To that end, I've begun researching various antidepressants. I ran into tianeptine when I was doing Power of the Poppy: apparently addicts in Armenia, Russia and the former Soviet Union have taken to shooting up large quantities of crushed Coaxil tablets to get an "opiate-like" high. (For those reading, this is a bad idea. Those who don't believe me should do an image search on "Russia Skeletor girl coaxil" if they're not at work and have a very, very strong stomach). Yet I'm also seeing reports of tianeptine abuse from people seeking a stimulant effect and taking pretty hefty oral doamounts to achieve it. (One guy in Turkey was taking 3 grams a day: the typical dose is 12.5mg TID). So it's obviously not a case of "stimulant in small doses: tickles opiate receptors in big doses," although I suppose it could have different effects if it avoids first pass metabolism and goes straight into the bloodstream.
Theoretically speaking, an SSRE should have the exact opposite therapeutic effect of an SSRI and throw the patient into a pretty nasty depression. Yet most clinical studies suggest that tianeptine is at least as effective as most SSRIs and can sometimes be more useful in patients who don't respond to SSRIs. I've been able to find two theories for its efficacy: one is that it has effect on the glutamatergic system, and the other is that both SSREs and SSRIs ultimately lead to downregulation of the presynaptic autoreceptors. But to my chemically ignorant (if sometimes chemically altered) mind, it kinda sorta sounds like nobody really knows for sure exactly why SSREs do the exact same thing SSRIs do.
Is there anybody here who knows anything about this particular class of compounds and could toss out some ideas on why this chemical appears to act like an opiate, a mild stimulant, and an antidepressant despite what one might expect from its effects?
Theoretically speaking, an SSRE should have the exact opposite therapeutic effect of an SSRI and throw the patient into a pretty nasty depression. Yet most clinical studies suggest that tianeptine is at least as effective as most SSRIs and can sometimes be more useful in patients who don't respond to SSRIs. I've been able to find two theories for its efficacy: one is that it has effect on the glutamatergic system, and the other is that both SSREs and SSRIs ultimately lead to downregulation of the presynaptic autoreceptors. But to my chemically ignorant (if sometimes chemically altered) mind, it kinda sorta sounds like nobody really knows for sure exactly why SSREs do the exact same thing SSRIs do.
Is there anybody here who knows anything about this particular class of compounds and could toss out some ideas on why this chemical appears to act like an opiate, a mild stimulant, and an antidepressant despite what one might expect from its effects?
