I never noticed immediate changes from Zoloft either. 
I did. I felt better the morning after my first dose. I haz a speshul brain. 
Placebo effect. I am fairly certain that 24 hours on an SSRI would have no significant impact on brain chemistry.
I doubt it takes more than a few hours for it to reach your brain and bind to the serotonin transporters. It's the knock-on effects of the reuptake inhibition on the rest of the brain that take longer. Think of it this way; if you take an overdose of it, I'm betting it doesn't hit you a month later.
Of course not. My point being that inhibiting serotonin re-uptake is not adding serotonin. The process of achieving the end result takes time.
Kind of like how cocaine and methylphenidate don't add dopamine when they bind to the dopamine transporters, and thus take weeks to have a significant impact on brain chemistry?
Exogenous serotonin clearance was measured at about 8 minutes according to this and in particular this, which points towards a reasonably brisk release-reuptake cycle; the point of a neurotransmitter is to transmit a signal across a synaptic gap after all, so the release-reuptake cycle can't take too long if it's going to signal anything with shorter timescale requirements than the circadian rhythm. With a cycle frequency on the order of minutes, I'd expect a significant change in synaptic serotonin to occur in a small multiple of that once some of the transporters get plugged up, since plugging up the transporters doesn't stop neurons from continuing to manufacture it and release it from vesicles.
I like this particular analogy:
Serotonin is a biological signal: essentially, it passes particular messages between cells. Serotonin does this by attaching to specific ‘receptors’ embedded in the cells that it’s communicating with. Picture a high-security vault that can only be opened by someone pressing the palm of their hand against a scanner to authorize access. In essence, serotonin behaves like the hand, while its receptor is the scanner. Only serotonin can interact with its receptor to ‘activate’ it and pass on the intended message.
The important thing is that the signal (serotonin) and its receptor have to work together. It’s no good having a lot of signaling chemical around if it’s only got a few receptors to attach to: the lack of receptors will limit how quickly and widely its message can be passed on.
This is where SSRIs might really make a difference. Rather than keeping serotonin levels high by blocking its re-uptake from the bits of the body where it has its effect (as described earlier), it is now thought that SSRIs might also have their biological effect by increasing the number of receptors that are present in the body – so that the serotonin that’s available can pass on its message more efficiently.
We can imagine that it would take a group of ten football supporters a while to enter a football stadium if there’s just one turnstile for them to pass through. But it’d be much quicker if there were five or ten turnstiles. In a similar way, ten serotonin molecules will be able to pass on their message much more quickly if there are ten receptors for them to bind to rather than if they’re all trying to compete for a single receptor.
However, it takes time to for our bodies to manufacture new receptors and install them at the right locations in our cells. And this explains why, even if SSRIs boost levels of serotonin in the body pretty quickly, the benefit of taking the antidepressant isn’t felt for some time. The extra serotonin molecules need to wait until more receptors have come on stream before the signals they transmit can get ‘louder’, leading to a rebalancing of mood.
http://www.oxfordmhf.org.uk/blog/2012/03/why-do-antidepressants-take-so-long-to-work/
