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. 2009 Oct 21;29(42):13242–13254. doi: 10.1523/JNEUROSCI.3376-09.2009

Figure 1.

Figure 1.

Ischemic injury causes rapid disruption of the AIS cytoskeleton, but not nodes of Ranvier. A, Coronal, contralateral sections of cortex from 6 h MCAO treated mouse, labeled with a Nissl stain (NeuroTrace, red) to detect neuronal cell bodies, Hoechst (blue) to label nuclei, and anti-βIV spectrin (green) to label the AIS. The white arrow indicates the location of the pial surface. The inset shows a higher magnification of a neuron with a βIV spectrin-positive AIS (arrow). B, Ipsilateral, injured cortex from 6 h MCAO treated mouse. Labeled as in A. The dashed line delineates the border of AIS staining. The inset shows higher magnification of neurons without βIV spectrin immunoreactivity. Note that a few neurons in the ischemic region retain their AIS βIV spectrin immunoreactivity. C, Coronal, contralateral sections of Striatum from 6 h MCAO treated mouse, labeled as in A. Boxes indicate regions of higher magnification shown in E, F. D, Ipsilateral, injured striatum from 6 h MCAO treated mouse. Labeled as in A. Boxes indicate regions of higher magnification shown in G, H. Note the complete absence of AIS βIV spectrin immunoreactivity, but preserved nodal βIV spectrin staining. Scale bar, 50 μm. E, F, Higher magnification of contralateral striatum shown in C to illustrate βIV spectrin immunostaining at the AIS (E) and nodes of Ranvier (F). G, H, Higher magnification of ipsilateral striatum shown in D to illustrate loss of βIV spectrin immunostaining from the AIS (G) and nodes of Ranvier (H). Scale bars: A–D, 50 μm.