to increase in aggressive strains of mice and in mice that have just engaged in aggressive behavior (e.g., Bernard et al., 1975; Modigh, 1973). With regard to specific brain regions, isolation-induced aggressive behavior in mice has been reported to increase DA levels in the striatum (Tizabi et al., 1979); DA uptake in the prefrontal cortex, but not striatum (Hadfield, 1981, 1983); and DA turnover in striatum (Hutchins et al., 1975), frontal cortex, and hypothalamus (Tizabi et al., 1979); hypothalamic DA levels were also elevated in attacking rats (Barr et al., 1979). In mice attacking for the first time, DA turnover in the nucleus accumbens is increased, but not after multiple aggressive experiences (Haney et al., 1990).
When mice or rats defend against attacks, several limbic forebrain structures show elevated metabolite levels of DA (Mos and van Valkenburg, 1979; Louilot et al., 1986; Puglisi-Allegra and Cabib, 1990). Defensive reactions to electric shock are also correlated with increased DA uptake in striatum (Hadfield and Rigby, 1976), and increased DA turnover in cortical and limbic areas (Dantzer et al., 1984).
Rats that kill mice do not significantly differ from so-called nonkillers in limbic DA but may differ slightly in hippocampal DA (Broderick et al., 1985; Barr et al., 1979); muricidal rats may also show increased DA metabolite levels (Tani et al., 1987).
The activity of brain dopamine undergoes large changes subsequent to either aggressive or defensive behavior. At present, different experimental preparations have implicated all three major forebrain dopamine systems (i.e., nigrostriatal, mesolimbic, and mesocortical). Brain dopamine systems appear to be particularly significant in (1) the reinforcing or rewarding aspects of violence and aggression, possibly via the mesolimbic and mesocortical DA systems, and/or (2) the neural mechanisms for initiation, execution, and termination of violent or aggressive behavior patterns, possibly via the nigrostriatal and mesolimbic DA systems. In order to assess these possibilities, it will be important to apply methodology with greater temporal, anatomically, and behaviorally differentiating resolution.
The evidence from studies with humans on the role of NE in neural mechanisms responsible for violent and aggressive behavior is limited to measurements of noradrenergic activity in the
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