Aggression is suppressed by acute stress but induced by chronic stress: Immobilization effects on aggression, hormones, and cortical 5-HT1B/ striatal dopamine D2 receptor density

Although it has been established by a number of investigators that a variety of stressors are associated with the induction
of aggressive behavior, two specific issues remain unanswered. First, it is unclear whether the contexts surrounding stressors
(e.g., stressor length and chance of winning over opponents) change outcomes regarding aggressive behavior. Second, if a relationship
exists between stress and aggressive behavior, altered levels of stress-related hormone (e.g., corticosterone [CORT]), as
well as aggression-related biomarkers (e.g., testosterone [T], density of prefronto-cortical 5-HT_1B receptor and striatal dopamine D₂ receptor [D2r]) may contribute to changes in aggressive behavior. Thus, we examined how immobilization (with a 1-, 5-, or
10-day exposure) would impact (1) a longitudinal course of aggression toward different-sized opponents, (2) levels of CORT
and T, and (3) densities of 5-HT_1B receptor (5-HT1Br) in the prefrontal cortex (PFC) and D2r in the striatum. It was found that, regardless of small or large
opponents, a single 2-h exposure to immobilization reduced aggressive behavior (stress-suppressed aggression) over time, whereas repeated (10-day) exposure to immobilization escalated aggressive behavior (stress-induced aggression). These stress effects persisted up to 1 week of recovery from immobilization stress. Moreover, immobilized rats demonstrated
elevated levels of T, but not CORT, as compared with controls. Finally, acute immobilization altered D2r densities in the
shell of the nucleus accumbens, and chronic immobilization changed 5-HT1Br in the PFC, including the downregulation of 5-HT1Br
densities in the right prelimbic and orbitolateral cortices. The potential relationships among stress, aggression, and 5-HT1Br/D2r
roles are discussed.