Serotonin and Suicidal Behaviora

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Abstract
Studies of the brain of suicide victims indicate there is a decrease in brain stem levels of 5-HT and/or 5-HIAA. There also appears to be a region-specific increase in 5-HT2 receptors, which are post synaptic and may therefore be increased in number secondary to decreased serotonin levels. Lack of information about how 5-HT2 and other serotonin receptor populations are regulated hamper our ability to explain the mechanisms underlying these findings. If the initial reports of a decrease in the number of imipramine binding sites prove to be correct then this finding would be further evidence for an effect involving the serotonin neurons, seen in this case at the level of the terminals. The relationship between suicide attempters and completers remains to be worked out. However, studies of suicide attempters, particularly those making more lethal attempts, appear to confirm the findings made in the brain of suicide completers. Neuroendocrine and CSF studies indicate the presence of serotonin subresponsivity and lower levels of CSF 5-HIAA. Thus, the overall direction of change is towards a weaker serotonin signal which rather than being due to a primary receptor defect (a possibility that cannot be ruled out but for which there is no current evidence), appears to be due to reduced levels of serotonin release. The causes of this effect represent a research challenge. It is clear that reduced levels of serotonin alone cannot explain the timing and type of suicidal behavior. Future studies must address the role of other neurotransmitters which may explain why some aggression is directed outward (towards other people) and in other cases the aggression is directed toward the self (suicidal behavior). Defining the role of serotonin and other involved transmitter systems is a necessary step before a comprehensive pharmacological treatment plan can be designed and tested.