SSRIs are fairly unique, and there are a number of hand wavey explanations for why their onset of mood altering effects is delayed.
The oldest one that I remember is the claim that antidepressant effects are due to autoreceptor downregulation. Basically, autoreceptors are located on the presynaptic neuron and measure synaptic neuro transmitter levels. They induce release when levels are low and inhibit release when levels are high. This theory states that ssris are less functional early on due to serotonin 1 auto receptors responding to increased serotonin levels.
Chronic selective serotonin reuptake inhibitor (SSRI) administration to rodents desensitizes or downregulates raphe 5-HT[1A] autoreceptors. We previously found elevated 5-HT[1A] binding in antidepressant-naïve and not recently-medicated major ...
www.ncbi.nlm.nih.gov
A more recent claim is that ssris are directly interacting with trkb receptors to increase bdnf signaling. The delay of action is explained by the fact that the interaction is very low affinity and it takes weeks of steady state dosing to achieve proper concentrations in the brain compartment. Trkb receptors are activated by bdnf and promote neuron growth. Their activation is correlated with antidepressant effects of many drugs of diverse classes.
It is unclear how binding of antidepressant drugs to their targets gives rise to the clinical antidepressant effect. We discovered that the transmembrane domain of tyrosine kinase receptor 2 (TRKB), the brain-derived neurotrophic factor (BDNF) receptor that promotes neuronal plasticity and...
pubmed.ncbi.nlm.nih.gov
I prefer the second theory.