Major depressive disorder is estimated to affect 4–6% of adolescents, and selective serotonin reuptake inhibitors (SSRIs) are the first-line pharmacotherapy in children and adolescents. However, there has been concern that adolescents starting treatment are at increased risk for developing suicidal ideation and in 2004, the US Food and Drug Administration issued a ‘black box’ warning on SSRI prescribing to children. As a result, rates of SSRI prescribing dropped worldwide, but there was little evidence to suggest that this had a protective effect. In 2003/4 suicide rates in adolescents increased for the first time in a decade (Gibbons et al, 2007). However, clinical trials have limited use in detecting suicide risk as completed suicide is so rare an event that no instances of suicide and few genuine attempts are ever captured in these studies. In light of these difficulties, alternate methods for addressing this question are needed. Because many behavioral and physiological responses are preserved across species, a translational research approach may be useful in this respect.

Although suicide is a complex behavior that is extremely difficult to reproduce in animal models, it may be possible to identify proximal biological mechanisms that mediate suicidal behavior. For instance, if the biological underpinnings of impulsivity, anxiety, or depression linked to SSRI administration can be modeled in animals, and those same variables are linked to increased suicidality, animal models can point toward candidate biological mediators of increased suicidality following SSRI administration. In the following paragraphs we comment on the findings of an article published in this issue of Neuropsychopharmacology (West et al, this issue), which compares the effect of an SSRI on brain function and behavior in juvenile and adult rodents. We highlight the important contribution this study makes to the field of suicidality, depression, and antidepressant treatment.

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