Figure 1

(a) The focal necrotic infarct region resulting from 30-minute transient MCAo (magnification 20×). In all cases in which a focal necrotic infarct region could be identified, it was subcortical with diffuse penumbral effects spanning cortically. (b) Evidence for penumbral damage spanning into the cortex as indicated by IBA-1 immunoreactivity (a marker for macrophages) in layer V of primary motor cortex in the lesioned hemisphere, (c) compared to the intact hemisphere. (d) Histogram depicting loss of large neurons in layer V of the motor cortex expressed as percent intact hemisphere (ANOVA p < 0.01) supported by representative images of H&E-stained sections from (e) the lesioned hemisphere and (f) the intact hemisphere. (g) Histogram depicting a trend towards caspase 3 activation in large neurons in layer V of the motor cortex expressed as fold change lesioned/intact (ANOVA, p > 0.05) supported by representative images of sections labelled with antibodies directed against active caspase 3 (BD Pharmingen) from (h) the lesioned hemisphere and (i) the intact hemisphere. Dotted white lines indicate layer V. (j) Microglial activation in the corticospinal tract contralateral to MCAo. (k) Active caspase 3-poitive neurons in the corticospinal tract contralateral to MCAo. Dotted lines in b-c, e-f, and h-i indicate layer V. Dotted lines in j-k indicate the spinal cord midline. All images taken at magnification 40× prior to reproduction unless noted.