Figure 3.

Hypoxic-ischemic injury is associated with significant alterations to astroglial coverage accompanied by changes in astrocyte morphology. Representative image of astrocytes labelled with glial fibrillary acidic protein (GFAP). (A) Astrocytes in C animals displayed long extended processes and small cell bodies, typical of resting astrocytes. (B, C) In the first 4H following insult, the cell bodies of the astrocytes began to hypertrophy, with gradual loss of the fine tertiary processes. (D, E) Between 4-8H, the primary processes began to thicken, followed by a distinct reorganization of the secondary processes seen at 12H. (F) The 24H group had few secondary processes, profoundly hypertrophied primary processes, and cell bodies. The scale bar equals 20 μm (A–F). Representative images of astrocyte coverage (GFAP) in the intragyral (G–L) and paraventricular (M–R) white matter regions. The scale bar indicates 250 μm (G–R). Quantification of GFAP expression using densitometry showed a decrease in GFAP expression in 2H, 4H, 12H and 24H groups in the intragyral white matter (S), and 24H group in the periventricular white matter (T). Column graphs illustrate the mean with error bars at one standard deviation. Statistical comparisons refer to ordinary one-way analysis of variance test with a two-stage linear step-up procedure of Benjamini, Krieger and Yekutieli. Statistical significance was accepted at q < 0.05 (^∗q < 0.05, ^∗∗q < 0.01, ^∗∗∗q < 0.001, ^∗∗∗∗q < 0.0001). C control group; Ctx cortex; DAPI’ 4′6-diamidino-2-phenylindole; FC, frontal cortex; GFAP, glial fibrillary acidic protein; (number)H, group culled hours post injury; IGWM, intragyral white matter; NeuN, neuronal nuclei; PVWM, periventricular white matter.