While reading these two papers, I found I was most interested
in the differing characterizations of what an animal model of depression looks
like, and of how it should be evaluated. When I read the description of the
numerous behavioral tests used in Bessa et al. I was immediately struck by how
thoroughly they demonstrated that the symptoms experienced by the rats
paralleled those seen in humans with depression. In other research papers I’ve
read it has been clear that while some symptoms can be adequately mimicked in
rats, often animal models of human diseases fall short of fully capturing the
disorder. In fact, what seemed to define the conflicting conclusions set forth
by these to papers was not a disagreement in the accuracy of data, but in the
accuracy of what can be considered a measure of depression. Santarelli et al.
based their conclusion on the assumption that NSF performance was sufficient to
demonstrate that a rat is experiencing something comparable to depression seen
in humans. Bessa et al., on the other hand, argued that NSF measures
anxiety-like behaviors only, and while anxiety is correlated with depression,
it cannot be used as a measure of depressive-like behaviors as a whole, or of
how well an antidepressant is working. In my opinion, by widening the range of
evaluations done to include the sucrose preference test to assess anhedonia and
the forced swimming test to measure learned helplessness, Bessa et al. were
able to define a stronger rat model of depression which encompassed symptoms
that better mirror human experiences, and therefore reach a more accurate
conclusion on the role neurogenesis plays in antidepressant effectiveness. Because
of this major difference between the papers, both groups were able to prove the
same point, that neurogenesis is essential for the anxiety-reducing behavioral
effects of antidepressants, and yet come to opposite conclusions about what this means, a situation which
I find fascinating and certainly worth remembering.
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