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Post 1- Neurogenesis & Anti-depressant Actions

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The two papers by Santarelli et al and Bessa et al aim to investigate the impact that antidepressants have on behavioural effects towards depressive disorders in relation to neurogenesis and neuronal plasticity. The treatment of antidepressants (ADs) discussed include fluoxetine, imipramine, desipramine, halodperidol, vehicle, and two putative antidepressants. Although the findings of the two appear concise, Santarelli et al do not present methodology in a similar coherent manner as Bessa et al, which may reduce its comprehensiveness somewhat. In contrast, Bessa et al present an extensive section indicating the materials and methodology used (such as the subjects, conditions and measurement technologies/tests).
 In the research conducted by Santarelli et al, emphasis is placed on the neurotransmitters serotonin (5HT) and noradrenaline (NA), claimed to increase in levels as a response to antidepressants. This may indicate enhancement in brain mobilization but also an improvement in appetite, as these are the predominant roles of the neurotransmitters. Bessa et al do not discuss these neurotransmitters as abundant. However, they instead investigated anhedonia each week with use of a sucrose preference test. In depressed subjects, when anhedonia was reduced and treated with antidepressants, which in turn increase serotonin levels (and influences appetite), there was an improvement in the sucrose preference test result. Bessa et al state that chronic mild stress can influence behavioural responses in relation to ADs. They also challenge Santarelli’s belief of neurogenesis being a direct cause to behavioural effects of antidepressants. Their findings instead suggest that even when there is a blockage in neurogenesis (tested with MAM), there is still evidence towards efficiency in alleviating depressive symptoms with ADs. Bessa et al thereby claim that neuronal plasticity, dendritic and spine density is a larger influence to depressive behaviour than neurogenesis.  With more focus on the biochemical imbalances of the neurotransmitters involved in the monoamine hypothesis (serotonin, dopamine, norepinephrine), Bessa et al would be adding more up to date findings building upon the previous research by Santarelli et al. 
In summary, reading the two papers created a greater understanding towards how different publications can build on each other over time. These two studies provide more coherent and supportive evidence to a common treatment such as antidepressants used in mice and its potential effect on human patients. Behavior is certainly affected by antidepressant treatment, thus the main contrast between the two findings is their respective causal factors within the brain. 

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