Citation

Kamali M, Oquendo MA, Mann JJ. Depress. Anxiety 2001; 14(3): 164-176.

Copyright

(Copyright © 2001, John Wiley and Sons)

DOI

10.1002/da.1062

PMID

unavailable

Abstract

Our current knowledge about the neurobiology of suicide is still limited. Technical limitations and the complexity of the CNS are major obstacles. However, there is evidence for a hereditary disposition to suicide, which appears to be independent of diagnosis. Clinical, postmortem, genetic, and animal studies suggest that serotonin has a central role. The main regions of interest in the CNS have been the dorsal and median raphe nuclei in the midbrain that host the main serotonergic cell bodies and the prefrontal cortex, particularly the ventral PFC, innervated by the serotonergic system. In vivo and postmortem studies indicate serotonergic hypofunction in suicide and serious suicide attempts. This deficiency in turn can lead to a predisposition to impulsive and aggressive behavior, probably due to a breakdown in the inhibitory function of the ventral prefrontal cortex as a result of less serotonin input. In the context of this predisposition and the development of mental illness or other life stressors, the individual is at risk of acting on suicidal thoughts. Such deficient serotonin input into the PFC may arise as a result of genetic, parenting, head injury, and other effects. Identifying psychiatric, social, and environmental predictors of suicide are studied to improve prediction and prevention of suicide. A better understanding of the neurobiology of suicide can help detect at risk populations and help develop better treatment interventions. Depression and Anxiety 14:164–176, 2001. © 2001 Wiley-Liss, Inc.