The efficacy of anti-depressant medications (ADs) has been a prevalent topic of discussion amongst cellular biologists and neuroscientists alike since the development of the drugs themselves. Particularly, researchers have been searching tirelessly to determine the precise neural correlate of depressive behaviors. The only unambiguous finding of this search has been the association of a marked increase in hippocampal neurogenesis that accompanies chronic AD treatments; however, researchers have been unable to directly pinpoint the functional significance of this activity. Thus, in order to identify the functional importance of increased hippocampal neurogenesis in response to chronic AD medication, Santarelli et al. examined the effects of radiological disruption of anti-depressant-induced hippocampal neurogenesis. The team performed X-irradiation on only the hippocampus of mice using a lead plate to direct the signal. The X-irradiation deactivated the neurogenic effect of the chronic AD medication, yielding no behavioral response to the ADs. Thus, Santarelli et al. found that disrupting this hippocampal neurogenesis entirely blocked any behavioral response to the anti-depressant medications, making the mice unresponsive to the ADs and nulling the functionality of the treatment.This study provides evidence for the notion that neurogenesis in the hippocampus is strongly-correlated to the behavioral effects of chronic anti-depressant treatment. Essentially, this indicates that chronic AD treatment MUST stimulate hippocampal neurogenesis, and without this stimulation, the behavioral response to chronic AD treatment will be nullified. Therefore, neurogenesis in the hippocampus is integral to the efficacy of chronic anti-depressant treatments, and these results are extremely significant because human beings respond most to chronic --not acute-- AD treatments.
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