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健康个体和反社会个体的行为抑制和奖励的神经相关性和 5-羟色胺能调制。

Neuronal correlates and serotonergic modulation of behavioural inhibition and reward in healthy and antisocial individuals.

机构信息

Sir Colin Alan Campbell Building, Institute of Mental Health, Section of Forensic Mental Health, University of Nottingham Innovation Park, Triumph Road, Nottingham NG7 2TU, UK.

出版信息

J Psychiatr Res. 2010 Feb;44(3):123-31. doi: 10.1016/j.jpsychires.2009.07.005. Epub 2009 Aug 14.

DOI:10.1016/j.jpsychires.2009.07.005
PMID:19683258
Abstract

Individuals with antisocial personality disorder (ASPD) are impulsive and show impairment in reinforcement processing. There is increasing evidence for a neurobiological basis of psychopathy, which shares some of the characteristics of ASPD, but research on the neuronal correlates of neuropsychological processes in ASPD remains limited. Furthermore, no research has examined the effects of serotonergic manipulation on brain activations in antisocial groups. In this study, 25 male participants with ASPD (mean age 42.1) and 32 male control participants (mean age 30.5; 25 participants providing usable scans) were randomly allocated to receive the 5-HT(2C)-agonist mCPP or placebo. Participants were scanned using functional magnetic resonance imaging (fMRI) during a behavioural inhibition (Go/NoGo) and a reward task. In comparison to healthy controls the ASPD group showed reduced task related activations in the dorsolateral prefrontal cortex (DLPFC) but increased signal in the pre/subgenual anterior cingulate cortex (ACC) in the Go/No-Go task and increased activation in OFC in the reward task. mCPP modulated brain responses in both tasks in the whole group. Interactions between group and drug occured in bilateral OFC, caudate and ventral pallidum during the reward task but no significant interactions were found in the Go/No-Go task. This suggests that ASPD involves altered serotonin modulation of reward, but not motor inhibition pathways. These findings suggest that ASPD involves altered DLPFC, ACC and OFC function. Altered serotonergic modulation of reward pathways seen in the ASPD group raises the possibility that targeting serotonin systems may be therapeutic.

摘要

具有反社会人格障碍(ASPD)的个体冲动,并且在强化处理方面表现出障碍。越来越多的证据表明,精神病态具有神经生物学基础,它具有一些与 ASPD 相同的特征,但对 ASPD 中神经心理学过程的神经元相关性的研究仍然有限。此外,没有研究检查 5-羟色胺能操作对反社会群体大脑激活的影响。在这项研究中,25 名男性 ASPD 参与者(平均年龄 42.1)和 32 名男性对照组参与者(平均年龄 30.5;25 名参与者提供了可用的扫描)被随机分配接受 5-HT(2C)激动剂 mCPP 或安慰剂。参与者在行为抑制(Go/NoGo)和奖励任务中使用功能磁共振成像(fMRI)进行扫描。与健康对照组相比,ASPD 组在 Go/No-Go 任务中背外侧前额叶皮层(DLPFC)的任务相关激活减少,但在前扣带皮质(ACC)的前/下皮质区域的信号增加,在奖励任务中眶额皮层(OFC)的激活增加。mCPP 在整个组的两个任务中都调节了大脑反应。在奖励任务中,在双侧 OFC、尾状核和腹侧苍白球中发生了组间和药物间的相互作用,但在 Go/No-Go 任务中没有发现显著的相互作用。这表明 ASPD 涉及到奖励的 5-羟色胺调节改变,但不是运动抑制途径。这些发现表明,ASPD 涉及到 DLPFC、ACC 和 OFC 功能的改变。在 ASPD 组中观察到的奖励途径中 5-羟色胺能调节的改变增加了靶向 5-羟色胺系统可能具有治疗作用的可能性。

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