Here's how I conceptualize it. Since serotonin and the other neurotransmitters are generally only released on demand (i.e., in response to an action potential), it isn't constitutively being released by pre-synaptic neurons into the synaptic cleft. I wouldn't think of neurotransmitters as being under the same kind of negative feedback as, say, the hormones of the HPA axis for example. Instead, they are simply synthesized and stored until use. By blocking the receptor on the post-synaptic neuron you are essentially preventing serotonin from doing anything while "waiting out" whatever stimulus is causing the serotonin to be released in the first place or, if something like a carcinoid, until it can be resected.
With chronic use I imagine you get some compensatory feedback (i.e., upregulation of post-synaptic receptors or increased serotonin synthesis), but I don't think you would see that kind of feedback acutely (like in serotonin syndrome).
Keep in mind that I'm not scoring 90% on UW in my first pass so you probably can't trust this.
Sent from my Nexus 7
