Administration of antidepressants initiates with up-regulation of target receptor sites along with many, many non-target receptor sites. Over time, those target receptors down-regulate and that is what is theorized to contribute to the antidepressant effect.
The period of initial antidepressant use and its associated up-regulation of receptors can increase activation, anxiety and akathisia, a feeling of intense physical discomfort and restlessness, with many people finding the anxiety and akathisia to be inescapable. One receptor associated with this is the 5HT2C subtype, which is not a targeted receptor, but still is activated as a side-effect of SSRI therapy.
It's hypothesized that people might harm themselves in order to decrease or escape the discomfort they feel while beginning antidepressants. Another hypothesis is that the anxiety and activation might drive someone who is struggling with suicidal thoughts to act upon them before the antidepressant's therapeutic effects kick in.
One of the reasons Prozac is approved for minors is 1) it has an extremely long half-life such that a missed dosed isn't the end of the world and 2) it antagonizes the 5HT2C receptor site, theoretically minimizing activation, anxiety and akathisia associated with starting an antidepressant regimen.