Dodds Chris M, Müller Ulrich, Clark Luke, van Loon Anouk, Cools Roshan, Robbins Trevor W
Behavioral and Clinical Neuroscience Institute, University of Cambridge, Cambridge CB2 3EB, United Kingdom.
J Neurosci. 2008 Jun 4;28(23):5976-82. doi: 10.1523/JNEUROSCI.1153-08.2008.
Complete understanding of the neural mechanisms by which stimulants such as methylphenidate ameliorate attention deficit hyperactivity disorder is lacking. Theories of catecholamine function predict that the neural effects of stimulant drugs will vary according to task requirements. We used event-related, pharmacological functional magnetic resonance imaging to investigate the effects of 60 mg of methylphenidate, alone and in combination with 400 mg of sulpiride, on blood oxygenation level-dependent (BOLD) signal in a group of 20 healthy participants during probabilistic reversal learning, in a placebo-controlled design. In a whole-brain analysis, methylphenidate attenuated BOLD signal in the ventral striatum during response switching after negative feedback but modulated activity in the prefrontal cortex when subjects maintained their current response set. The results show that the precise neural site of modulation by methylphenidate depends on the nature of the cognitive subprocess recruited.
目前尚缺乏对诸如哌甲酯等兴奋剂改善注意力缺陷多动障碍的神经机制的完整理解。儿茶酚胺功能理论预测，兴奋剂药物的神经效应会根据任务要求而有所不同。我们采用事件相关的药理功能磁共振成像，在一项安慰剂对照设计中，研究了60毫克哌甲酯单独使用以及与400毫克舒必利联合使用时，对20名健康参与者在概率性逆转学习过程中血氧水平依赖（BOLD）信号的影响。在全脑分析中，哌甲酯在负反馈后的反应切换过程中减弱了腹侧纹状体的BOLD信号，但在受试者维持当前反应集时调节了前额叶皮质的活动。结果表明，哌甲酯调节的确切神经部位取决于所招募的认知子过程的性质。
