(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus.

В статье представлены результаты количественного и морфологического анализ нейронов у мышей в области ишемического поражения, через 6 часов после внутрисосудистой окклюзии средней мозговой артерии (MCAO). Продемонстрировано разделение области поражения на ишемический очаг и ишемическую полутень. Показано изменение морфологии клеточных тел и ядер нейронов в ишемическом очаге. The article presents the results of a quantitative and morphological analysis of neurons in mice in the area of ischemic injury, 6 hours after intravascular occlusion of the middle cerebral artery (MCAO). The division of the affected area into an ischemic focus and an ischemic penumbra was demonstrated. Changes in the morphology of cell bodies and nuclei of neurons in the ischemic focus are shown.

Проведен цитологический анализ изменения морфологии микроглиоцитов в мозге мышей, перенесших локальную ишемию головного мозга посредством окклюзии средней мозговой артерии (MCAO). Описана специфика изменения морфологии микроглиоцитов в белом и сером веществе головного мозга в ипсилатеральном полушарии. It was performed the cytological analysis of microglia morphology in mice underwent focal ischemia by means of middle cerebral artery occlusion (MCAO). The features of morphological microglyocyte changes in a white and gray matter of ipsilateral lesioned hemisphere was described.