Studer Erik, Näslund Jakob, Andersson Erik, Nilsson Staffan, Westberg Lars, Eriksson Elias
Department of Pharmacology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, POB 431, SE 405 30 Gothenburg, Sweden.
Mathematical Sciences, Chalmers University of Technology, SE 412 96 Gothenburg, Sweden.
PLoS One. 2015 May 15;10(5):e0126462. doi: 10.1371/journal.pone.0126462. eCollection 2015.
The sex hormone testosterone and the neurotransmitter serotonin exert opposite effects on several aspects of behavior including territorial aggression. It is however not settled if testosterone exerts its pro-aggressive effects by reducing serotonin transmission and/or if the anti-aggressive effect of serotonin requires the presence of the androgen. Using the resident intruder test, we now show that administration of the serotonin synthesis inhibitor para-chlorophenylalanine (300 mg/kg x 3 days) increases the total time of attack as well as the percentage amount of social behavior spent on attack but not that spent on threat - i.e. that it induces a pattern of unrestricted, maladaptive aggression - in gonadectomized C57Bl/6 male mice receiving testosterone replacement; in contrast, it failed to reinstate aggression in those not given testosterone. Whereas these results suggest the pro-aggressive effect of testosterone to be independent of serotonin, and not caused by an inhibition of serotonergic activity, the pCPA-induced induction of maladaptive aggression appears to require the presence of the hormone. In line with these findings, pCPA enhanced the total time of attack as well the relative time spent on attacks but not threats also in wild-type gonadally intact male C57Bl/6 mice, but failed to reinstate aggression in mice rendered hypo-aggressive by early knock-out of androgen receptors in the brain (ARNesDel mice). We conclude that androgenic deficiency does not dampen aggression by unleashing an anti-aggressive serotonergic influence; instead serotonin seems to modulate aggressive behavior by exerting a parallel-coupled inhibitory role on androgen-driven aggression, which is irrelevant in the absence of the hormone, and the arresting of which leads to enhanced maladaptive aggression.
性激素睾酮和神经递质血清素在包括领地攻击性在内的行为的多个方面发挥着相反的作用。然而,睾酮是否通过减少血清素传递来发挥其促进攻击的作用,和/或血清素的抗攻击作用是否需要雄激素的存在,目前尚无定论。使用定居者-入侵者测试,我们现在表明,给予血清素合成抑制剂对氯苯丙氨酸(300mg/kg×3天)可增加攻击总时间以及用于攻击的社会行为的百分比,但不会增加用于威胁的社会行为的百分比——也就是说,它会在接受睾酮替代的去势C57Bl/6雄性小鼠中诱导一种不受限制的、适应不良的攻击模式;相反,在未给予睾酮的小鼠中,它未能恢复攻击性。虽然这些结果表明睾酮的促攻击作用独立于血清素,并非由血清素能活性的抑制引起,但对氯苯丙氨酸诱导的适应不良攻击似乎需要激素的存在。与这些发现一致,对氯苯丙氨酸在野生型性腺完整的雄性C57Bl/6小鼠中也增加了攻击总时间以及用于攻击而非威胁的相对时间,但在通过早期敲除大脑中的雄激素受体而变得低攻击性的小鼠(ARNesDel小鼠)中未能恢复攻击性。我们得出结论,雄激素缺乏不会通过释放抗攻击的血清素能影响来抑制攻击;相反,血清素似乎通过对雄激素驱动的攻击发挥平行耦合的抑制作用来调节攻击行为,在没有激素的情况下这种作用无关紧要,而抑制这种作用会导致适应不良攻击增强。