Ferenczi Emily A, Zalocusky Kelly A, Liston Conor, Grosenick Logan, Warden Melissa R, Amatya Debha, Katovich Kiefer, Mehta Hershel, Patenaude Brian, Ramakrishnan Charu, Kalanithi Paul, Etkin Amit, Knutson Brian, Glover Gary H, Deisseroth Karl
Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.
Neurosciences Program, Stanford University, Stanford, CA 94305, USA.
Science. 2016 Jan 1;351(6268):aac9698. doi: 10.1126/science.aac9698.
Motivation for reward drives adaptive behaviors, whereas impairment of reward perception and experience (anhedonia) can contribute to psychiatric diseases, including depression and schizophrenia. We sought to test the hypothesis that the medial prefrontal cortex (mPFC) controls interactions among specific subcortical regions that govern hedonic responses. By using optogenetic functional magnetic resonance imaging to locally manipulate but globally visualize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, whereas locally increased mPFC excitability reduces this striatal response and inhibits the behavioral drive for dopaminergic stimulation. This chronic mPFC overactivity also stably suppresses natural reward-motivated behaviors and induces specific new brainwide functional interactions, which predict the degree of anhedonia in individuals. These findings describe a mechanism by which mPFC modulates expression of reward-seeking behavior, by regulating the dynamical interactions between specific distant subcortical regions.
对奖励的动机驱动适应性行为,而奖励感知和体验受损(快感缺乏)会导致包括抑郁症和精神分裂症在内的精神疾病。我们试图验证内侧前额叶皮质(mPFC)控制着调节享乐反应的特定皮质下区域之间相互作用的这一假设。通过使用光遗传学功能磁共振成像技术在局部操纵但全局可视化大鼠的神经活动,我们发现多巴胺神经元刺激驱动纹状体活动,而局部增强的mPFC兴奋性会降低这种纹状体反应,并抑制对多巴胺能刺激的行为驱动。这种慢性mPFC过度活动还会稳定地抑制自然奖励驱动的行为,并诱导特定的全脑新功能相互作用,这些相互作用可预测个体的快感缺乏程度。这些发现描述了一种机制,通过该机制mPFC通过调节特定远距离皮质下区域之间的动态相互作用来调节寻求奖励行为的表达。