How I understand the things:
5HT levels increase indeed at the time you take SSRI, but not sustainably, because of autoreceptors (5HT1A presynaptic and others), that,being activated with this additional 5HT, decrease serotonin synthesis and release in turn. It takes time for them to be desensitize. Then postsynaptic 5HT receptors such as 5HT2C, 5HT7 and others need time to down-regulation, after which side effects subside and therapeutic 5HT1A(postsynaptic)-mediated effect develops fully. 5HT1A induce dopamine and oxytocin release among other. And further effects include nerve cells regrowth via BDNF raise, boost of enkephaline synthesis etc. That's why the delay is.
As for opioids, they disinhibit mesolimbic dopamine release, that is highly pleasurable. You just can't experience SA or depression being in such a state of bliss. Stims like cocaine do ultimately the same, but through another mechanism. In contrast to them, opioids calm you down by parallel cAMPH synthesis suppression (something opposite to caffeine action).