Focusing on the Santarelli et al. article.

Focusing on the Santarelli et al. article.

The article’s aim was to investigate whether an increase in neurogenesis is required for AD findings. 

                  First I am going to briefly discuss the methods that showed circumstances in which AD’s had some sort of recorded effect on the mice. Firstly the AD’s showed effect in the adapted version of the NSF test, where chronic use of AD’s (SSRI and TDAs only) showed to have effect by a decreased latency to eat food, but acute treatment did not have any effect with AD treatment, mirroring the delay of AD effects in humans. The effect of fluoxetine similarly showed the distinction between chronic AD use and acute AD use; chronic AD use showed a substantial increase in BrdU-positive cells in the dentate gyrus, whereas acute use did not show an increase, causally projecting the use of AD with increased neurogenesis.

A similarity in decreased latency to feed was also obtained by chronic activation of 5-HT_1A receptors with the direct agonist 8-OH-DPAT, showing that the 5-HT_1A receptors are implicated in the modulation of anxiety related disorders. An interesting factor to note however is that 5-HT_1A  receptor knockout mice responded to TCAs but not the SSRI which suggests to us that both AD’s use independent molecular pathways.

AD use also showed circumstances in which there was no effect; for example (i) when they disrupted neurogenesis within the hippocampus and (ii) when the 5-HT_1A receptor was deleted, in turn the effects of all AD use were blocked in the first example and SSRI treatment was blocked in the second. 

 The article did also have a few notable dissociations, but on the whole the article managed to constructively show a strong link between behavior and neurogenesis and that there is a strong framework to build on in relation to stimulating hippocampal neurogenesis and the treatment of anxiety and depressive disorders.