Prozac, or fluoxetine, boosts serotonin levels. When the scientists exposed 2C-receptor BNST neurons to Prozac, it increased the effect of the 2C-receptor neurons on the neighboring VTA- and LH-projecting neurons. The mice became more fearful and anxious.
To find out how to stop this effect, senior author Thomas L. Kash and his team focused on the anxiety-mediating BNST neurons. They noticed that these neurons expressed a molecule, known as corticotropin releasing factor (CRF). CRF is a stress-signaling neurotransmitter. It is sometimes called corticotropin releasing hormone (CHR).
When the team added a compound to block CRF activity, the fear and anxiety that had been triggered by the Prozac were greatly reduced.
Searching for a solution
Kash believes the same thing would happen in humans. SSRIs can cause anxiety in people, he says, and mice and humans tend to have very similar pathways in these brain regions.