Serotonin and Aggression

摘要: Abstract Traditional clinical research on the neurobiology of aggressive behavior focuses individuals who are characterized by their impulsive, hostile, antisocial and violent traits show some deficiency in brain serotonin (5-HT) activity relative to those have a propensity engage premeditated, calculating instrumental acts. Preclinical has focused territorial, dominant or maternal patterns, chiefly for reproductive purposes. Recent efforts study very high levels due genetic selection, consumption moderate dose alcohol, social instigation pharmacological insults. The early proposal that lower CSF 5-HT and/or 5-HIAA were associated with greater outbursts (the ‘serotonin hypothesis’) been challenged evidence implicating receptor subtypes 1 2 families, transporter (5-HTT) metabolic enzyme monoamine oxidase A (MAOA), acting at different neuroaxis. In vivo techniques revealed significant role cortical release during termination an confrontation its consequences, rather than initiation. Considerable preclinical implicates 1A , 1B 2A as targets pharmacotherapeutic management escalated behavior, which accompanied varying extent non-specific effects, whereas data linking these receptors specific types aggression less consistent. prevalent anti-aggressive effects emerge drugs targeting 5-HTT, from human non-human primates suggest short allele 5-HTT polymorphism risk factor traits, particularly combination environmental stress. Contrary inhibition MAO, mutation MAOA gene humans mice suggests chronically elevated may promote most prominently after life maltreatment. Interactions between polymorphisms complex epistatic interactions ultimately reveal strong phenotypes.