In the articles Santarelli et al. (2003) and Bessa et al. (2009), two points of view regarding the mechanisms of antidepressants on mammals is presented. Santarelli (2003) argues the point that the interaction between neurogenesis and antidepressants require time to have a full effect on the mammalian hippocampus, which is the only location on the human brain where neurogenesis has been observed.
The Santarelli group targeted a specific neurotransmitter receptor which, in previous studies to be directly associated with depression and anxiety. The measurement of anxiety, is something that I do not understand to be quantified in rodent experiments. Anxiety based on feeding patterns seems to be applicable, but the functional mechanisms of how depression works is still a mystery. Therefore, coupling of depression and anxiety to me are not interchangeable.
That being said, the Santarelli group showed a clear indication of the effect of Antidepressant drugs and the effect on behavior. They claimed that the time differential is due to the process of neurogenesis altering the structure of the hippocampus.
The Bessa group, six years later, claimed that there were more factors taking place in the effects of ADs on the hippocampus. They argued that neuroplasticity has a more prominent role in the effects of the drugs.
After both arguments were presented, my thoughts lie on the overall function of healthy brain activity. New memories are dependent on neuroplasticity, and the effects of neurogenesis are still not functionally proven. There are only two areas that show neurogenesis in one area of the brain. The idea that the growth of these neurons alone can change the entire behavior of an organism while the rest of the neurological system remains unaffected seems overly simplistic. I believe there to be a more overarching effect on the entirety of the nervous system that is being overlooked.