Clinical Neuroscience Research Unit, Department of Psychiatry, University of Chicago Pritzker School of Medicine, Chicago, IL 60637, USA.
J Clin Psychopharmacol. 2012 Jun;32(3):329-35. doi: 10.1097/JCP.0b013e31825368b7.
The mechanistic model whereby serotonin affects impulsive aggression is not completely understood. The purpose of this study was to test the hypothesis that depletion of serotonin reserves by tryptophan depletion affects emotional information processing in susceptible individuals.
The effect of tryptophan (vs placebo) depletion on processing of Ekman emotional faces was compared in impulsive aggressive personality disordered, male and female adults with normal controls. All subjects were free of psychotropic medications, medically healthy, nondepressed, and substance free. Additionally, subjective mood state and vital signs were monitored.
For emotion recognition, a significant interaction of Aggression × Drug × Sex (F(1, 31) = 7.687, P = 0.009) was found, with male normal controls but not impulsive aggressive males showing increased recognition of fear. For intensity ratings of emotional faces, a significant interaction was discovered of Drug × Group × Sex (F(1, 31) = 5.924, P = 0.021), with follow-up tests revealing that males with intermittent explosive disorder tended to increase intensity ratings of angry faces after tryptophan depletion. Additionally, tryptophan depletion was associated with increased heart rate in all subjects, and increased intensity of the subjective emotional state of "anger" in impulsive aggressive subjects.
Individuals with clinically relevant levels of impulsive aggression may be susceptible to effects of serotonergic depletion on emotional information processing, showing a tendency to exaggerate their impression of the intensity of angry expressions and to report an angry mood state after tryptophan depletion. This may reflect heightened sensitivity to the effects of serotonergic dysregulation, and suggests that what underlies impulsive aggression is either supersensitivity to serotonergic disturbances or susceptibility to fluctuations in central serotonergic availability.
血清素影响冲动攻击的机制模型尚未完全阐明。本研究旨在检验这样一个假设，即色氨酸耗竭导致血清素储备耗竭会影响易感个体的情绪信息处理。
在冲动型攻击性人格障碍的男性和女性成年患者中，与正常对照组相比，通过色氨酸（与安慰剂相比）耗竭来比较处理艾克曼情绪面孔的效果。所有患者均未服用精神药物、身体健康、无抑郁且未滥用物质。此外，还监测了主观情绪状态和生命体征。
在情绪识别方面，发现了一个显著的交互作用，即攻击×药物×性别（F(1, 31) = 7.687，P = 0.009），正常对照组的男性而非冲动型攻击性男性表现出对恐惧的识别能力增强。对于情绪面孔的强度评分，发现了药物×组别×性别的显著交互作用（F(1, 31) = 5.924，P = 0.021），进一步的测试表明，间歇性爆发障碍的男性在色氨酸耗竭后，愤怒面孔的强度评分往往会增加。此外，色氨酸耗竭会导致所有患者的心率增加，以及冲动型攻击性患者的“愤怒”主观情绪状态的强度增加。
具有临床相关水平的冲动攻击性的个体可能容易受到血清素耗竭对情绪信息处理的影响，表现出夸大对愤怒表情强度的印象以及在色氨酸耗竭后报告愤怒情绪状态的倾向。这可能反映了对血清素调节紊乱的敏感性增加，并且表明冲动攻击的基础要么是对血清素紊乱的超敏感性，要么是对中枢血清素可用性波动的易感性。
