Santarelli el al Study

 A brief glance at the Santarelli article brought up the question of whether an increase in neurogenesis is needed to see the effects of antidepressant treatments. The mechanism by which antidepressants work is by increasing the amount of serotonin (5-HT) and/or noradrenaline (NA). Although antidepressant treatments rapidly increase levels of these neurochemicals, the effect of the treatment is not seen until three to four weeks afterwards, suggesting a delay in neurochemical structural changes is needed to see the effects of the treatment.

            The methodology of the study focused experimentally answering the multifaceted approach to the question of whether neurogenesis is needed to effectively administer antidepressants. The experiments identified the effects of antidepressant usage between chronic and acute usage. In an adapted version of the NSF test, chronic antidepressant usage (for SSRI and TDAs) showed a decreased in latency to eat food, whereas acute usage did not have any effect. Another distinction made between chronic and acute usage was the increasing levels of BrdU-positive cells in the dentrate gyrus with chronic antidepressant usage. Acute antidepressant usage did not show significant increase leading to the idea that increased usage of antidepressants coincide with increased neurogenesis.

            The decrease in latency to feed was also seen when activating 5-HT_1A receptors with the agonist 8-OH-DPAT. In the NSF test, 5-HT_1A receptor KO mice did not respond to the SSRI fluoxetine but responded to TCA antidepressants (imipramine and desipramine). This finding was important that it highlighted the activation of 5-HT_1A receptors is important to SSRIs. The results indicated that serotonin and norepinerine enhancing antidepressants act through independent pathways. It is also important to note that the deletion of the 5-HT_1A receptors led to the absence of both behavioral and neurogenic effects (when tested with fluoxetine).

            The study in Santarelli el al concluded that stimulating neurogenesis in the hippocampal region of the brain can lead to reversing atrophy that is prevalent in depression/anxiety disorders which can be done by certain antidepressants.