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Abstract #10244 Published in IGR 6-1
Ischemia-induced alterations of AMPA-type glutamate receptor subunit: expression patterns in the rat retina: an immunocytochemical study
Dijk F; Kamphuis WBrain Research 2004; 997: 207-221
This study investigates whether retinal ischemia/reperfusion leads to alterations in the expression of AMPA-type glutamate receptor (AMPAR) subunits GluR1-4. In ischemia-vulnerable hippocampal neurons, a subunit-specific downregulation of GluR2 precedes the actual neurodegeneration. The purpose was to study whether retinal ischemia induces a similar downregulation of GluR2 preceding the loss of ganglion and amacrine cells. A 60-min ischemic period was followed by reperfusion lasting between two hours and seven days. Changes in the expression patterns of GluR1-4 were assessed using immunocytochemistry. In the same sections, alterations in cell density, thickness of retinal layers, and density of apoptotic cells were investigated. Two-hour post-ischemia, GluR1 immunoreactivity was nearly absent from the inner plexiform layer (IPL). Thereafter, labeling intensity recovered slowly and was close to control levels at seven days, albeit in a thinner IPL. The decrease in GluR2/3 labeling intensity was most profound at four hours. The recovery of GluR2/3 staining intensity was slow, and staining was still decreased at seven days. GluR2 immunoreactivity was not attenuated after ischemia. GluR4 labeling showed a similar time course as observed for GluR1, but the decrease in immunoreactivity was less profound and the recovery was nearly complete. The immunostaining of PKC α, a rod bipolar cell marker, was unaffected at all reperfusion times. The reduction of GluR staining preceded both the typical thinning of the IPL and the peak of cell loss, but coincided with a significant swelling of the IPL. In conclusion, retinal ischemia/reperfusion leads to differential changes in the expression of the different AMPA-type GluR subunits, which may affect excitatory synaptic transmission in the inner retina. However, no evidence was found for a preferential loss of GluR2 immunoreactivity that could account for selective neurodegeneration of amacrine and ganglion cells after retinal ischemia.
Dr. F. Dijk, Glaucoma Research Group, Netherlands Ophthalmic Research I, Graduate School the Neurosciences Amsterdam, Meibergdreef 47, 1105 BA, Amsterdam, the Netherlands
Classification:
2.13 Retina and retinal nerve fibre layer (Part of: 2 Anatomical structures in glaucoma)
3.3 Immunohistochemistry (Part of: 3 Laboratory methods)
