Retinal glia rapidly phosphorylate ERK1/2 after RGC axotomy.

<p>(<b>a–d</b>) p-ERK immunoreactivity in neurons (<b>a</b>) In uninjured retinas there is expression of ERK1/2 in all cellular compartments, both in neuronal and in non-neuronal cells, detected with an antibody to total ERK1/2. Total ERK1/2 staining continued to be expressed to the same level in retinas at days 1 and 3 post-axotomy (data not shown). (<b>c</b>) In uninjured retinas ERK1/2 is phosphorylated in RGCs. (<b>b</b>) At day 1 after ON axotomy, there was a robust increase of p-ERK1/2 immunoreactivity in putative glial cells in the GCL, INL, and both plexiform layers. Note the relative reduction of p-ERK1/2 in the GCL versus control normal retinas. (<b>d</b>) At day 3 after ON axotomy both the soma and the processes of retinal glia are robustly labeled with p-ERK1/2. Note that, unlike what was shown for p-Akt, the glial fibers with p-ERK1/2 point both towards the injured RGCs and towards the photoreceptors (full arrows). Arrowheads point to the soma of glia. (<b>e,f</b>) p-ERK immunoreactivity in glia. (<b>e</b>) p-ERK is strongly expressed in the end-feet, somas and processes of Müller cells expanding throughout the PhR layer rapidly after axotomy, as shown by co-localization of p-ERK with CRALBP. (<b>f</b>) The expression of p-ERK was low in astrocytes, as revealed by the weak co-localization of p-ERK with GFAP. GCL: ganglion cell layer; IPL: inner plexiform layer; INL: inner nuclear layer; PhR: photoreceptor layer. Scale bar, 30 µm.