Stanford Neurosciences Interdepartmental Program, Stanford University School of Medicine, Stanford, CA, USA.
Department of Psychiatry, Brain Health Institute, Rutgers University, NJ, USA.
Commun Biol. 2024 Sep 19;7(1):1178. doi: 10.1038/s42003-024-06836-9.
The biological mechanisms that contribute to cocaine and other substance use disorders involve an array of cortical and subcortical systems. Prior work on the development and maintenance of substance use has largely focused on cortico-striatal circuits, with relatively less attention on alterations within and across large-scale functional brain networks, and associated aspects of the dopamine system. Here, we characterize patterns of functional connectivity in cocaine use disorder and their spatial association with neurotransmitter receptor densities and transporter bindings assessed through PET. Profiles of functional connectivity in cocaine use disorder reliably linked with spatial densities of dopamine D receptors across independent datasets. These findings demonstrate that the topography of dopamine receptor densities may underlie patterns of functional connectivity in cocaine use disorder, as assessed through fMRI.
导致可卡因和其他物质使用障碍的生物学机制涉及一系列皮质和皮质下系统。先前关于物质使用的发展和维持的研究主要集中在皮质-纹状体回路上，而对大规模功能大脑网络内部和跨网络的变化以及多巴胺系统的相关方面关注较少。在这里，我们描述了可卡因使用障碍的功能连接模式及其与通过 PET 评估的神经递质受体密度和转运体结合的空间关联。可卡因使用障碍的功能连接模式的特征与多巴胺 D 受体的空间密度在独立数据集之间可靠相关。这些发现表明，多巴胺受体密度的拓扑结构可能是通过 fMRI 评估的可卡因使用障碍中功能连接模式的基础。
