We have previously observed changes in the RNA editing of AMPA receptors after acute spinal cord injury (SCI); this implies that post-transcriptional modifications are capable of affecting the physiological properties of glutamate receptor channels and related signal transduction in this neurodegenerative condition. Here, we report that the editing of the ionotropic KAR is markedly decreased at both GluK1 and GluK2 Q/R sites in the epicenter of the lesion and with distinct magnitude and kinetics also in the caudal and rostral portions of the injured cord. These effects are persistent, being observed as late as 30 days after lesioning. In addition, also the I/V and Y/C sites of GluK2 were severely affected after SCI. These findings add novel information to the relevance of editing of glutamate receptors following acute SCI, thus expanding the recently emerged role of post-transcriptional mechanisms under these experimental conditions.
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