Dynamic Interhemispheric Desynchronization in Marmosets and Humans With Disorders of the Corpus Callosum

• Main Authors: Diego Szczupak, Cecil C. Yen, Cirong Liu, Xiaoguang Tian, Roberto Lent, Fernanda Tovar-Moll, Afonso C. Silva, in collaboration with the IRC5 Consortium
• Format: Article
• Language: English
• Published: Frontiers Media S.A. 2020-12-01
• Series: Frontiers in Neural Circuits
• Subjects: cingulate cortex; corpus callosum; dynamic functional connectivity; dysgenesis of the corpus callosum; marmosets; non-human primates
• Online Access: https://www.frontiersin.org/articles/10.3389/fncir.2020.612595/full

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 (Callithrix jacchus) 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.