Center for Social and Affective Neuroscience, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.
Transl Psychiatry. 2018 Nov 30;8(1):264. doi: 10.1038/s41398-018-0316-2.
Major depressive disorder (MDD) is characterized by the altered integration of reward histories and reduced responding of the striatum. We have posited that this reduced striatal activation in MDD is due to tonically decreased stimulation of striatal dopamine synapses which results in decremented propagation of information along the cortico-striatal-pallido-thalamic (CSPT) spiral. In the present investigation, we tested predictions of this formulation by conducting concurrent functional magnetic resonance imaging (fMRI) and C-raclopride positron emission tomography (PET) in depressed and control (CTL) participants. We scanned 16 depressed and 14 CTL participants with simultaneous fMRI and C-raclopride PET. We estimated raclopride binding potential (BP), voxel-wise, and compared MDD and CTL samples with respect to BP in the striatum. Using striatal regions that showed significant between-group BP differences as seeds, we conducted whole-brain functional connectivity analysis using the fMRI data and identified brain regions in each group in which connectivity with striatal seed regions scaled linearly with BP from these regions. We observed increased BP in the ventral striatum, bilaterally, and in the right dorsal striatum in the depressed participants. Further, we found that as BP increased in both the left ventral striatum and right dorsal striatum in MDD, connectivity with the cortical targets of these regions (default-mode network and salience network, respectively) decreased. Deficits in stimulation of striatal dopamine receptors in MDD could account in part for the failure of transfer of information up the CSPT circuit in the pathophysiology of this disorder.
重度抑郁症（MDD）的特征是奖赏历史的整合改变和纹状体反应减少。我们假设 MDD 中纹状体激活减少是由于纹状体多巴胺突触的持续刺激减少，导致皮质-纹状体-苍白球-丘脑（CSPT）螺旋上的信息传播减少。在本研究中，我们通过对抑郁和对照（CTL）参与者同时进行功能磁共振成像（fMRI）和 C-raclopride 正电子发射断层扫描（PET）来测试这一表述的预测。我们对 16 名抑郁患者和 14 名对照者进行了扫描，同时进行 fMRI 和 C-raclopride PET。我们以体素为单位估计 raclopride 结合潜力（BP），并根据纹状体中的 BP 比较 MDD 和 CTL 样本。使用显示组间 BP 差异显著的纹状体区域作为种子，我们使用 fMRI 数据进行全脑功能连接分析，并确定每组中与纹状体种子区域的连接与这些区域的 BP 呈线性关系的大脑区域。我们观察到抑郁组双侧腹侧纹状体和右侧背侧纹状体的 BP 增加。此外，我们发现 MDD 中左腹侧纹状体和右背侧纹状体的 BP 增加，与这些区域皮质靶区（默认模式网络和突显网络）的连接减少。MDD 中纹状体多巴胺受体刺激不足部分可以解释该疾病病理生理学中 CSPT 电路信息传递失败的原因。
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