We believe that our results may provide a valuable contribution to the discussion of the role of CREB in antidepressant drug action and depression, noting that CREB-dependent regulation of neurotrophin responses observed after some antidepressants can be associated not only with the neuronal structures traditionally regarded as important key players in depression pathology but also directly in the neurotransmitter targets of antidepressant therapies. This evidence concerns the gene BDNF and depressive symptom measurement.