Neurogenesis and Anxiety - Emily Jones
The previous posts bring up a really good point in criticizing the generalizability of Santarelli and
colleagues’ results. Bessa et al. (2009) looked at multiple dimensions of depression while
Santarelli et. al. (2003) only examined anxiety-like feeding behavior and then generalized their findings.
Intuitively, it seems that the later 2009 paper contains more conclusive results: that it is neuronal
remodeling that is necessary for the behavior improving actions of antidepressants. However, I think
Bessa and colleagues’ do not necessarily refute, but adds onto the work of Santarelli et al., helping
readers to evaluate the 2003 article in a new way. Bessa and colleagues’ findings corroborate the need
for neurogenesis but also, by examining different behavioral manifestations of depression, makes for a
more generalizable result when discussing the pathogenesis of depression.
Although the research done by Bessa et al. suggests that behavioral homeostasis is restored by
antidepressants are via neuronal remodeling, rather than neurogenesis, it is important to point out that
their findings do not overshadow that of Santarelli et al. Importantly, by corroborating the necessity of
neurogenesis in ameliorating anxiety-like behaviors, I believe both papers this week encourage further
research to be done studying neurogenesis especially in the context of ameliorating anxiety-like
behaviors specifically. The finding that neurogenesis is essential for the anxiolytic properties of
antidepressants in these two articles may not have major implications for treating clinical depression,
but may present promising routes for the study of the neurogenesis hypothesis on related anxiety
disorders including generalized anxiety and post-traumatic stress.
colleagues’ results. Bessa et al. (2009) looked at multiple dimensions of depression while
Santarelli et. al. (2003) only examined anxiety-like feeding behavior and then generalized their findings.
Intuitively, it seems that the later 2009 paper contains more conclusive results: that it is neuronal
remodeling that is necessary for the behavior improving actions of antidepressants. However, I think
Bessa and colleagues’ do not necessarily refute, but adds onto the work of Santarelli et al., helping
readers to evaluate the 2003 article in a new way. Bessa and colleagues’ findings corroborate the need
for neurogenesis but also, by examining different behavioral manifestations of depression, makes for a
more generalizable result when discussing the pathogenesis of depression.
Although the research done by Bessa et al. suggests that behavioral homeostasis is restored by
antidepressants are via neuronal remodeling, rather than neurogenesis, it is important to point out that
their findings do not overshadow that of Santarelli et al. Importantly, by corroborating the necessity of
neurogenesis in ameliorating anxiety-like behaviors, I believe both papers this week encourage further
research to be done studying neurogenesis especially in the context of ameliorating anxiety-like
behaviors specifically. The finding that neurogenesis is essential for the anxiolytic properties of
antidepressants in these two articles may not have major implications for treating clinical depression,
but may present promising routes for the study of the neurogenesis hypothesis on related anxiety
disorders including generalized anxiety and post-traumatic stress.
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