Long prelude: Maybe a year ago I read an article on the web about SSRE's, or selective serotinin reuptake enhancers, being used for depression, asthma , premature ejaculation and some other diseases. Tianeptine, or trade name stablon is approved in Europe but not in the US. My uncle asked me about it at that time and I had no clue, I had to look it up. I have always thought the mechanism of action of SSRI's is this: inhibiting the reuptake of seroronin making it more available at the neurosynapse. But something always did not add up: Why did some SSRI's work and others didn't for some patients? Correct me if I'm wrong, but serotonin's concentration in the synapse does increase from day 1, but the effect (anti-depressant, for eg) cannot be appreciated for 2-3 weeks, right? Which means, according to theory, that new neuronal connections have to be established (or at least that is the reason of the delay). So then, what is teh role of serotonin? I asked the above question in bold to a few psychiatrists, they didn't know. So now with SSRE's (here's a link from wikipedia, google for more ( http://en.wikipedia.org/wiki/Tianeptine), HOW DO antidepressant SSRI's or SSRE's work? Surely it is not serotinin mediated. I just find it funny that they still have serotonin in the acronym SSRI/E, when a serotonin's uptake can't be both enhanced and inhibited AND cause the same result: eg better mood. Any input?