The δ2 glutamate receptor (GluRδ2) 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 GluRδ2 regulates cerebellar LTD have remained elusive. Because a mutation occurring in lurcher mice causes continuous GluRδ2 channel activity that can be abolished by 1-naphtylacetylspermine (NASP), a channel blocker for Ca2+- permeable iGluRs, GluRδ2 is thought to function as an ion channel. Here, we introduced a mutant GluR δ 2 transgene, in which the putative channel pore was disrupted, into GluR δ2 -null Purkinje cells using a virus vector. Surprisingly and similar to the effect of the wild-type GluR δ2 transgene, the mutant GluR δ2 completely rescued the abrogated LTD in GluR δ2-null mice. Furthermore, NASP did not block LTD induction in wild-type cerebellar slices. These results indicate that GluRδ2, a member of the iGluR family, does not serve as a channel in the regulation of LTD induction.
ASJC Scopus subject areas