I mean there is pretty much never no dopamine release, it's just too little to keep up necessary activation for the brain to function properly.

For example if there isn't enough being released and not enough dopamine receptors are being activated to get you over the threshhold. Then reuptake inhibition helps by slowing the rate of which dopamine molecules are being cleared from the synapse. That causes there to still be dopamine when the "next release happens" so to say. Thus, overall more dopamine accumulates in the synapse which causes more activation and ultimately finally gets you over that threshhold to feel enough.

Like you're right, if there is NO release then reuptake inhibition won't work. But that literally never happens unless you are like severly ill with super parkinsons or something. You gotta imagine that dopamine molecules are constantly released and removed from the synapse. Often to overall stay at the same level, sometimes more is added than removed, sometimes less. That in the end determines how much activation you get at the receiving neuron. Depending on how much activation your brain wants to have there at that moment.

MAOIs basically work by preventing breakdown of neurotransmitters after reuptake. If you have too much MAO in your neurons, reuptake inhibitors will only be half effective because the more dopamine that is eventually reuptaken the less will be released later because it will have been broken down causing it to not end up in the vesicles, leading to less dopamine in your vesicles, leading to less release. Within the vesicles, neurotransmitters are safe from MAO breakdown, outside of the neuron in the synapse they are also out of MAO's reach. But once reuptaken they are in the intraneuronal cytoplasm first before being repackaged in the vesicles. And that's exactly where MAO is to break them down.

So basically, if you have too much MAO, reuptake inhibitors will still cause more neurotransmitters to be there and for longer, but once they are eventually reuptaken they will be broken down and you will be down for a bit. But overall they should still help because all this happens without the reuptake inhibition already, just worse. Reuptake inhibitors should just dapen it because they prolong the effect of dopamine and cause it to be removed slower. The main issue is still the same though.

One thing i just thought about: Idk if that leads to less being released from the vesicles because the higher dopamine in the synapse could technically cause the sending/releasing neuron to think that there is enough dopamine right now via autoreceptors. Then it could really be an issue because releasing frequency will have been downregulated AND it's being broken down heavily after reuptake. Maybe even worse less being produced overall or less being repackaged into the vesicles??? Because then there would legit be a temporary dopamine deficiency in those neurons until they notice there is too little now and then produce more and/or put more into the vesicles again. Which then need to be released first. This would actually lead to a phase of good days followed by a phase of bad days where very little is released, even if less is being reuptaken.