Fig. 5

Ultrastructural characteristics of microglia and astrocytes during subacute phase of post-stroke inflammation. Representative transmission electron microscopy images of capillaries, neurons, microglia, and astrocytes in the peri-infarct area of stroke, at 7 and 21 days after dMCAO, in the inhibitor and control animals. a–d At 7 days post-dMCAO, perivascular M/Ms were seen in the vicinity of the microvessels. Note the signs of significant phagocytic activity of the perivascular microglia in the control group, with characteristic large lysosomal inclusions in the cytoplasm (c, d). e–h Perineuronal microglial cells were seen adhered to the healthy-looking neurons in the inhibitor group (e, f) and damaged necrotic neurons in the control group (g, h), at 7 and 21 days after dMCAO. Microglia nuclei contained distinctly accumulated dense heterochromatin. g Microglial cell invaded the damaged neuron. Neuronal cytoplasm has dispersed and disrupted organells and swollen mitochondria. i–l Swollen activated perineuronal and perivascular astrocytes were seen in both groups, at 7 and 21 days after dMCAO. The astrocytes were characterized by dispersed residual organelles and swollen mitochondria. Astrocyte fusion was often observed (k). m, n Significant edema and neuronal necrosis were observed at 21 days in control animals, with multiple necrotic neurons, collapsed blood vessels, and heavily vacuolated brain tissue (n). In contrast, visibly less damaged brain tissue was observed in the animals from the inhibitor group. Note healthy-looking neurons, intact and functional microvessels, and overall normal appearance of neuropil (m). M microglia/macrophage, BV blood vessel, EC endothelial cell, Per pericyte, Lys lysosome, L lipofuscin-like deposit, N neuron, A astrocyte, *—astrocytic process, m—mitochondria. Bars: a–h 1 μm; i–l 2 μm, and m, n 5 μm. Original magnifications: a–l ×1500–7000 and m, n ×800