Department of Neurobiology, University Pittsburgh Brain Institute, University of Pittsburgh, Pittsburgh, PA, United States.
Cerebral Microcirculation Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States.
Front Neural Circuits. 2020 Dec 21;14:612595. doi: 10.3389/fncir.2020.612595. eCollection 2020.
The corpus callosum, the principal structural avenue for interhemispheric neuronal communication, controls the brain's lateralization. Developmental malformations of the corpus callosum (CCD) can lead to learning and intellectual disabilities. Currently, there is no clear explanation for these symptoms. Here, we used resting-state functional MRI (rsfMRI) to evaluate the dynamic resting-state functional connectivity (rsFC) in both the cingulate cortex (CG) and the sensory areas (S1, S2, A1) in three marmosets () with spontaneous CCD. We also performed rsfMRI in 10 CCD human subjects (six hypoplasic and four agenesic). We observed no differences in the strength of rsFC between homotopic CG and sensory areas in both species when comparing them to healthy controls. However, in CCD marmosets, we found lower strength of quasi-periodic patterns (QPP) correlation in the posterior interhemispheric sensory areas. We also found a significant lag of interhemispheric communication in the medial CG, suggesting asynchrony between the two hemispheres. Correspondingly, in human subjects, we found that the CG of acallosal subjects had a higher QPP correlation than controls. In comparison, hypoplasic subjects had a lower QPP correlation and a delay of 1.6 s in the sensory regions. These results show that CCD affects the interhemispheric synchrony of both CG and sensory areas and that, in both species, its impact on cortical communication varies along the CC development gradient. Our study shines a light on how CCD misconnects homotopic regions and opens a line of research to explain the causes of the symptoms exhibited by CCD patients and how to mitigate them.
胼胝体是大脑两半球之间主要的神经结构，控制着大脑的侧化。胼胝体发育畸形（CCD）可导致学习和智力障碍。目前，这些症状没有明确的解释。在这里，我们使用静息态功能磁共振成像（rsfMRI）评估了三只自发性 CCD 狨猴的扣带回皮质（CG）和感觉区（S1、S2、A1）的动态静息态功能连接（rsFC）。我们还对 10 名 CCD 人类受试者（6 名发育不全和 4 名发育不全）进行了 rsfMRI 检查。当与健康对照组相比时，我们在两种物种中均未发现同型 CG 和感觉区之间 rsFC 强度的差异。然而，在 CCD 狨猴中，我们发现后半球间感觉区准周期模式（QPP）相关性的强度较低。我们还发现内侧 CG 中存在半球间通讯的显著滞后，表明两个半球之间存在不同步。相应地，在人类受试者中，我们发现无胼胝体受试者的 CG 与对照组相比具有更高的 QPP 相关性。相比之下，发育不全的受试者的 QPP 相关性较低，在感觉区滞后 1.6 秒。这些结果表明，CCD 会影响 CG 和感觉区的半球间同步性，并且在两种物种中，其对皮质通讯的影响沿着 CC 发育梯度而变化。我们的研究揭示了 CCD 如何使同型区域失连，并开辟了一条研究途径，以解释 CCD 患者的症状的原因，并探讨如何减轻这些症状。
