Depression is associated with a deficit of serotonin (5-HT), one of the neurotransmitters essential for communication between neurons and particularly involved in eating and sexual behaviours, the sleep-wake cycle, pain, anxiety and mood problems.

Odile Kellermann and Jean-Marie Launay's research, published in the Journal Science today, shows that Prozac effects a microRNA (miR-16) that is involved in the manufacture of the serotonin transporter. The serotonin transporter's role is to remove serotonin from the synapse.

Under normal conditions, this transporter is present in  "serotonergic" neurons, (i.e. neurons that produce serotonin). However, miR-16 normally prevents "norepinephrine" neurons from producing this transporter. norepinephrine is another neurotransmitter involved in attention, emotions, sleep, dreaming and learning.

In response to Prozac, the serotonergic neurons release a signal molecule, which causes the quantity of miR-16 to drop, which unlocks expression of the serotonin transporter in the norepinephrine neurons.

These norepinephrine neurons become sensitive to Prozac. They continue to produce norepinephrine, but they also start to make serotonin.

In other words, Prozac works by preventing serotonin from being removed from the synapse and by causing norepinephrine neurons to start making serotonin as well. The reason it takes up to three weeks is that 3 weeks is how long it takes for the changes to take place in the norepinephrine neurons.