Animal Models Review

In these two papers, Santarelli et al. (2003) and Bessa et al. (2009) study whether neurogenesis is required for antidepressant action.  The former believe that progenitor cells are required for antidepressants to work.  The latter believe that they are not necessary, and instead, that antidepressants induce neurogenesis.  Santarelli et al. (2003) tried to prove that hippocampal neurogenesis participated in the mechanism of antidepressants.  They pointed out that irradiation of brain regions, except for the hippocampus, did not alter the behavioral response to antidepressants.  In addition, they found that the grooming and feeding latency of irradiated mice did not decrease when treated with serotonergic and noradrenergic antidepressants.  However, by irradiating the entire hippocampus, Santarelli et al. (2003) could not point to a specific cause or mechanism by which antidepressants had no effect on the mouse. Bessa et al. (2009) hypothesized that neuronal plasticity and neurogenesis are not mutually exclusive.  Antidepressant treatments correlated with many examples of neuroplasticity in the brain, as evidenced by how they restored synaptic connections and dendritic growth.  In accordance with Santarelli et al. (2003), they found that neurogenesis seems to be necessary for the anxiolytic properties of antidepressants.  However, they did not reach that conclusion for its antidepressant properties.  I found the Bessa et al. (2009) paper more convincing as they confirmed positive behavioral, molecular, structural, and genetic effects of antidepressants on the hippocampus and pre-frontal cortex. 

            I think that the next step is to immunostain for neural progenitor cells in the hippocampus to see how many there are in rats with and without depression and in rats with SSRI treated depression.  This will give a more specific, numerical reference from which to keep studying the impact that neurogenesis has on the treatment of depression and vice versa.