

The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery.





The research is weakened by its reliance on observations of cells in culture rather than in actual patients. The SSRI dose typically delivered to a patient’s brain is actually a fraction of what is swallowed in a pill. “Obvious next steps are showing that what we found here is indeed viewed in patients as well,” Shomron says.

The study turned up additional drug targets for treating depression—two microRNA molecules, miR-221 and miR-222. Essentially, microRNAs are small molecules that can turn a gene off by binding to it. The microarray results showed a significant decrease in the expression of miR-221 and miR-222, both of which are predicted to target ITGB3, when cells were exposed to paroxetine. So, a drug that could prevent those molecules from inhibiting the production of the ITGB3 protein would arguably enable the growth of more new neurons and synapses. And, if the neurogenesis and synaptogenesis hypothesis holds, a drug that specifically targeted miR-221 or miR-222 could bring sunnier days to those suffering from depression.