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

Abstract

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 stressrelated 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 D 2 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.

Lipoic acid and pentoxifylline mitigate nandrolone decanoate-induced neurobehavioral perturbations in rats via re-balance of brain neurotransmitters, up-regulation of Nrf2/HO-1 pathway, and down-regulation of TNFR1 expression

“…In harmony with the present findings, McGinnis (2004) reported that androgenic anabolic steroids may sensitize rats to their surroundings and lower aggression threshold. The crucial role played by androgens as mediators of aggression is emphasized by eliminated aggression in castrated rats (Bergvall and Hansen, 1990;Yohe et al, 2012). Rats are normally known to defend their territory in…”

Neurochemical correlates of accumbal dopamine D2 and amygdaloid 5-HT1B receptor densities on observational learning of aggression

“…Alternatively, the downregulation of D2R following chronic passive exposure to aggression may be subject to increased dopamine release in the AcbSh, which would be an intrinsically rewarding/salient signal for observer rats. In contrast, note that chronic stress is not associated with a compensatory downregulation of D2R density in the AcbSh immediately after stress (Lucas, Wang, McCall, & McEwen, 2007) or even after a recovery period (Lucas et al, 2004; Yohe et al, 2012). Accordingly, our findings were less likely to be confounded with any social stress effect (Tzanoulinou, Riccio, de Boer, & Sandi, 2014; Wommack & Delville, 2007), as no group difference was observed in the levels of serum corticosterone immediately following passive exposure (see Table 1).…”

“…This is primarily because it was necessary to check stress hormone corticosterone levels following exposure before hormone levels returned to baseline. Given that stress potentially induced aggression (Wood, Norris, Waters, Stoldt, & McEwen, 2008; Wood, Young, Reagan, & McEwen, 2003; Yohe, Suzuki, & Lucas, 2012), the present protocol was helpful in confirming whether acute and chronic exposure to aggression did not produce unexpected stress. Furthermore, the present protocol helped us clarify whether any change in the target receptor density occurred slowly (e.g., in 24 hours following exposure session; see Suzuki et al (2010a, 2010b)), or rapidly (e.g., even immediately following exposure session).…”

Repeated restraint stress enhances cue-elicited conditioned freezing and impairs acquisition of extinction in an age-dependent manner

“…This is further supported by anxiogenic effect of CRF in both human and animal studies, and that many affective disorders, such as depression and posttraumatic stress disorder, are accompanied by increased concentration and responsiveness of CRF [56–58]. Other neurotransmitter systems, such as dopamine, norepinephrine and serotonin are sensitive to the effects of stress, and may contribute to the effects of stress on amygdala function [59–63]. …”