ABSTRACT
Neurobiological research in human aggression stems mainly from systematic manipulations of central neurotransmitters in different animal models of aggression. Animal behavioral studies have indicated that increasing or decreasing serotonin (5-HT) activity pharmacologically produces decreases or increases in aggression, respectively (Soubrie, 1986). It is notable that human data coincide with those suggested by animal research because there is considerable clinical evidence that links impulsive-aggressive behaviors in adults to reduced brain 5-HT function (Coccaro & Kavoussi, chap. 4, this volume). Similar relationships between aggression and brain 5-HT function may exist in children and adolescents in view of continuities from childhood to adulthood in both aggressive behavior and in central 5-HT function. One of the clearest findings concerning adolescent and adult aggressive and antisocial behavior is that such behavior is predictable statistically from early antisocial, aggressive, and hyperactive behavior (Cairns, Cairns, Neckerman, Ferguson, & Gariépy, 1989; Farrington, 1990; Huesmann, Eron, Lefkowitz, & Walder, 1984; Moffitt, 1990; Olweus, 1979; Pulkkinen & Pitkanen, 1993). The more aggressive child is likely to become both the more aggressive adult and the more antisocial and criminal adult. Although the development of the serotonergic system is difficult to characterize, there is relatively good intraindividual stability over the life cycle for concentrations of the principal 5-HT metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in cerebrospinal fluid (CSF) (Leckman et al., 1980; Shaywitz, Cohen, Leckman, Young, & Bowers, 1980; Traskman-Bendz, Asberg, Bertilsson, & Thoren, 1984).
