^That's not really the same thing actually in my opinion. Low levels of monoamines are not the direct cause of depression, but likely just a secondary effect caused by something else. With that being said we don't need more compounds that increase dopamine, noradrenaline, and serotonin levels no matter what their mechanism is. Higher mood observed after DA/NE/5-HT releasers is not equal to curing depression. Honestly, it's a bit hard to debate if we don't really have a proper biochemical definition of depression.
SSRIs may actually not be effective in treating depression at all. The increased levels of serotonin as a result of SSRI treatment may increase mood but the healing process may be happening somewhere else, a higher mood may simply allow this healing process to happen or rather help it to be more likely to happen, but it won't necessarily happen and that's what we observe, SSRIs are not effective for everyone. The same actually applies SNRIs and NDRIs. I'm not really against 4-methylaminorex (I guess you mean 4,4'-dimethylaminorex?), but I honestly can't see the point. I can imagine the effectiveness would be around SSRIs/SNRIs and it wouldn't get us a single step closer to understanding depression.
The reason for considering buprenorphine as a treatment for depression is a bit different, I guess. It's something different enough to be researched. Kappa agonist salvinorin was found to cause depressive-like effect in rats (
source) and there are quite a few studies on the potential of kappa antagonists as antidepressants that you can easily find. This may still not be the direct treatment for depression fixing the cause, but I guess it's closer than using monoamine releasers/reuptake inhibitors which could be compared to shooting to a criminal who is somewhere among other people in the crowd. Kappa antagonists seem to be a more specific treatment.
Honestly, if there are people ruling this planet who really care, then why can't we have ketamine as a treatment? This drug was proved to work almost instantly with a much much better effectiveness than SSRIs. We've got potent painkillers stocked in pharmacies so ketamine having potential for causing addiction is not really a good excuse, especially if what a patient needs is a few doses at most which are a few times lower than common doses used recreationally. And the way ketamine works may be even more specific than buprenorphine's kappa antagonism.
The involvement of increased levels of acetylcholine in depression is also interesting and something fresh in the subject. (
link, I can't find the article itself though)
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")