Molecular plasticity of retinal ganglion cells after partial optic nerve injury

In the past few years we established the partial crush of the optic nerve as an in vivo model system for the study of signaling pathways involved in molecular plasticity after axonal injury. The simplicity of this model at the cellular level allows decisive questions to be answered whilst functional aspects of visual information processing can be studied in parallel. A major advantage of a partial optic nerve crush model is the opportunity to directly compare different cell populations: (i) the rapidly degenerating retinal ganglion cells (RGC), (ii)the axotomized RGC population that eventually dies over the period of the next few weeks, (iii) the axotomized RGC population surviving for a long time in the retina without an axon and (iv) the surviving RGC population that maintains axonal connections to their brain targets. Thus, differential aspects of post-lesion plasticity between axotomized and non-axotomized cells can be studied and gene transcription leading either to cell death or survival can be analyzed. Using this axonal injury model we investigated the expression of immediate early genes, glutamate receptors, and other differentially expressed genes that we identified with a combined subtractive hybridization and suppression polymerase chain reaction (PCR) screen. Moreover, we characterized time course of cell death, the astroglia response of the retina and optic nerve as well as the topography of anterograde acid retrograde axonal transport.