Abstract
Suicide is a serious public health problem in the US, yet its neurobiological underpinnings are poorly understood. Suicide is highly correlated with depressive symptoms, and considerable evidence suggests that depression is associated with a relative deficiency in serotonergic neurotransmission. Serotonergic circuits also mediate impulsivity, a trait obviously relevant to suicide. These findings, taken together, suggest that alterations in the serotonergic system might contribute to suicidal behavior, serving as an impetus for researchers to scrutinize the serotonin transporter (SERT) as a potential substrate for the pathophysiology of suicide. Using post-mortem brain tissue, platelets, and DNA from suicide completers and attempters have not provided unequivocal evidence for a pre-eminent role for the SERT in the pathophysiology of suicide. This paper provides a review of several studies that have evaluated the role of the SERT in the pathophysiology of suicide.
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Acknowledgements
Appreciation for guidance in the genetics of SERT is extended to our colleague Steven J Garlow MD, PhD. This work was supported by an Emory University-Abbott Laboratories Young Faculty Development Award to David C Purselle, NIH Grants MH-42088, MH-39415, MH-58922, and an Established Investigator Award from the American Foundation for Suicide Prevention to Charles B Nemeroff.
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Purselle, D., Nemeroff, C. Serotonin Transporter: A Potential Substrate in the Biology of Suicide. Neuropsychopharmacol 28, 613–619 (2003). https://doi.org/10.1038/sj.npp.1300092
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DOI: https://doi.org/10.1038/sj.npp.1300092
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