The delta2 glutamate receptor (GluRdelta2) belongs to the ionotropic glutamate receptor (iGluR) family and plays a crucial role in the induction of cerebellar long-term depression (LTD), a form of synaptic plasticity underlying motor learning. Nevertheless, the mechanisms by which GluRdelta2 regulates cerebellar LTD have remained elusive. Because a mutation occurring in lurcher mice causes continuous GluRdelta2 channel activity that can be abolished by 1-naphtylacetylspermine (NASP), a channel blocker for Ca(2+)-permeable iGluRs, GluRdelta2 is thought to function as an ion channel. Here, we introduced a mutant GluRdelta2 transgene, in which the putative channel pore was disrupted, into GluRdelta2-null Purkinje cells using a virus vector. Surprisingly and similar to the effect of the wild-type GluRdelta2 transgene, the mutant GluRdelta2 completely rescued the abrogated LTD in GluRdelta2-null mice. Furthermore, NASP did not block LTD induction in wild-type cerebellar slices. These results indicate that GluRdelta2, a member of the iGluR family, does not serve as a channel in the regulation of LTD induction.