2021/09/15
Yamagata University School of Medicine
Keio University School of Medicine
There are various types of neural plasticity related to neural functions, including memory and learning, and this includes plasticity in myelinated fibers involving oligodendrocytes. However, the detailed molecular mechanisms and functional significance of this oligodendrocyte-dependent plasticity have remained unclear. A joint research group led by Associate Professor Yoshihiko Yamazaki of the Department of Physiology, Yamagata University School of Medicine (including Professor Satoshi Fujii from the same department, Associate Professor Kenji Tanaka and Project Assistant Professor Yoshifumi Abe from the Department of Neuropsychiatry, Keio University School of Medicine) focused on a specific molecule expressed in oligodendrocytes—NKCC1—and investigated its relationship with oligodendrocyte-involved plasticity in mice. They found that during the juvenile period, neural plasticity is more enhanced compared to adulthood, and concurrently, NKCC1 expression is higher in the juvenile period than in adulthood. In mice lacking NKCC1, juvenile neural plasticity was attenuated, leading to the discovery that the expression level of NKCC1 in oligodendrocytes is closely associated with neural plasticity in myelinated fibers. Next, the research group investigated whether simply artificially increasing the reduced levels of NKCC1 in adulthood could restore neural plasticity to a level equivalent to that of the juvenile period. As a result of this manipulation, neural plasticity was enhanced even in adulthood, and learning ability was improved. These research findings suggest that the rejuvenation of brain function by targeting oligodendrocytes has become possible in animal models, and that this method could be a new strategy for improving brain function. The research results were published in the online edition of "Nature Communications" on August 26, 2021.
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