Santarelli et al. studied the role of anti-depressant
induced neurogenesis in treating depression-like behaviors. However, the
research from Bessa et al. suggests that anti-depressants treat depression
through neuronal remodeling, rather than neurogenesis.
To
determine the effects of antidepressants on depression-like behaviors in 5-HT1a
receptor knockout mice, Santarelli et al. used a novelty suppressed feeding test . Bessa et al. subjected Wistar rats to an unpredictable
chronic mild stress (CMS) paradigm and used the sucrose preference, forced
swim, and novelty suppressed feeding tests to assess depression-like behavior
in Wistar rats. They found that the paradigm increased depression-like
behaviors, but the symptoms were relieved after 1 week with imipramine and
after 2 weeks with fluoxetine.
Santarelli et al. used knockout mice to model depression. In
the discussion, the authors acknowledge the problems with using knockout mice;
the absence of the 5-HT1A receptor during development causes anxious
behavior. This could effect the results of their experiment, because the mice’s
behaviors could be because of the developmental deficit instead of the
depression model. Bessa
et al. used the CMS to induce depression-like symptoms in rats. This method has
a better translational value to humans than knockout mice. The authors stated
that the loss in hippocampal and PFC volume is similar to the reduction in volume
that depressed humans experience. In both rats and humans, the atrophy can be
reversed by chronic antidepressant treatment. This supports the idea that antidepressants
work through neuronal remodeling instead of neurogenesis. It is important for
anti-depressant researchers to do studies that are translational to humans so
we can create more effective treatments for patients with depression.
Santarelli et al. irradiated the SGZ of the mice to decrease
neurogenesis while administering antidepressants. However, Bessa et al. pointed out that
irradiation requires a recovery period before the mice can be given
antidepressants, which might affect the results of the experiment. Instead of
irradiation, Bessa et al. used MAM, a drug that reduces neurogenesis without
any noticeable health deficits.
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