system
Given the following post, respond as if you're commenting on Reddit:
human
How is it that both SSRIs and SSREs are both effective antidepressants, despite having the exact opposite mechanism of action?

Selective Serotonin Reuptake Inhibitors (SSRIs) supposedly increase the extracellular level of serotonin, while Selective Serotonin Reuptake Enhancers (SSREs) supposedly do the exact opposite. Yet both classes of drugs have been effectively used as antidepressants. What's going on here?

This seemingly paradoxical effect makes me wonder if perhaps we're getting this entire mechanism of action wrong. It's commonly believed that SSRIs treat depression and anxiety by increasing serotonin levels, which makes us feel better. In other words, more serotonin = better. But it's also known that SSRIs can often make things worse before they slowly get better. What if the real cause of eventual relief is **habituation** of serotonin receptors after being inundated with extra serotonin? What if serotonin is actually causing the problem?

This theory would explain why SSREs (or more specifically Tianeptine, the only SSRE currently on the market) have a much faster onset of action... they're addressing the problem by reducing serotonin levels. In other words, too much serotonin = bad, and SSREs attack this issue directly.

Of course, this is all a wild conspiracy theory on my part, and I'd love for someone to prove me wrong and explain how all this really works.

What say you, AskScience?
gpt
Theyre not necessarily opposite function. Ssri's increase the amount of serotonin in the synapse, which allows more serotonin to saturate receptors. Ssre's however, despite their name, do not increase serotonin to be removed from the synapse, they increase the sensitivity of serotonin receptors, meaning more serotonin is taken up which would other wise not be utilized by the receptors.