Fig. 1

Abnormal mitoses are common features of reactive astrogliosis. a Examples of astrocytes arrested in metaphase in excitotoxic (pilocarpine [neocortex] and kainic acid [hippocampus, CA1]), mechanical (stab wound [neocortex]), and ischemic [neocortex] brain damage. Note enlargement of astrocyte cell bodies, reduction of the numbers of main branches, and abnormal positions of metaphase chromosomes distributed over the entire volume of the cell bodies (black and white insets of DAPI stains in lower right segments of each panel). Immunostaining for GFAP, counterstaining with DAPI. Confocal microscopy. b Arrested mitoses in astrocytes (arrows, left 2 images) and astrocytes with many small nuclei (right 2 images). One day after BrdU (80 mg/kg) administration on day 3 after pilocarpine administration, piriform cortex. Confocal microscopy. c Schematic presentation of the most damaged brain areas after pilocarpine administration and the locations of arrested mitoses. Note in the right panels (immunostaining for GFAP) that areas of tissue damage (asterisks) in hippocampus and piriform cortex are devoid of GFAP immunostaining. d Time scale of the dynamics of astrocyte cycling after one BrdU dose (80 mg/kg, i.p.) given on day 3 after pilocarpine administration. Sections were examined 9–24 h after BrdU administration. e Example of ‘doublets’ when daughter astrocytes do not migrate away from each other after mitosis (arrow, note that neighboring nuclei are separated by plasma membranes visualized with GLAST) and when a mitosis was not followed by cytokinesis, generating a binucleated astrocyte (arrowhead, note that the nuclei are not separated by plasma membranes). Scale bars:  a = 10 μm, b = 45 μm, e = 20 μm