Cuprizone-induced oligodendrocyte loss and demyelination impairs recording performance of chronically implanted neural interfaces.

ABSTRACT: Biological inflammation induced during penetrating cortical injury can disrupt functional neuronal and glial activity within the cortex, resulting in potential recording failure of chronically implanted neural interfaces. Oligodendrocytes provide critical support for neuronal health and function through direct contact with neuronal soma and axons within the cortex. Given their fundamental role to regulate neuronal activity via myelin, coupled with their heightened vulnerability to metabolic brain injury due to high energetic demands, oligodendrocytes are hypothesized as a possible source of biological failure in declining recording performances of intracortical microelectrode devices. To determine the extent of their contribution to neuronal activity and function, a cuprizone-inducible mod

SUBMITTER: Wellman SM 

PROVIDER: S-EPMC7540937 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature