The ionotropic glutamate receptor subunit GluR6 undergoes developmentally a
nd regionally regulated Q/R site RNA editing that reduces the calcium perme
ability of GluR6-containing kainate receptors. To investigate the functiona
l significance of this editing in vivo, we engineered mice deficient in GIu
R6 Q/R site editing. In these mutant mice but not in wild types, NMDA recep
tor-independent long-term potentiation (LTP) could be induced at the medial
perforant path-dentate gyrus synapse. This indicates that kainate receptor
s with unedited GluR6 subunits can mediate LTP. Behavioral analyses reveale
d no differences from wild types, but mutant mice were more vulnerable to k
ainate-induced seizures. Together, these results suggest that GluR6 Q/R sit
e RNA editing may modulate synaptic plasticity and seizure vulnerability.