Functional analysis of GluD2 signal transduction

我们通过表型拯救方法对δ2谷氨酸受体（δ2）进行了功能分析。通过将δ2的N端突变体转导到δ2缺失的浦肯野细胞中，我们证明δ2的胞外N端区域对于平行纤维（PF）-浦肯野细胞（PC）突触的形成和/或维持是不可或缺的，但对于长时程抑制（LTD）不是不可或缺的，而长时程抑制是PF-PC突触的一种可塑性形式。我们还发现PTPMEG，一种与δ2的C-末端区域相互作用的酪氨酸磷酸酶，在LTD的诱导中使2型谷氨酸受体去磷酸化。

We performed functional analysis of the δ2 glutamate receptor (δ2) through phenotype-rescue method. By transducing an N-terminal mutant of δ2 into δ2-null Purkinje cells, we demonstrated that the extracellular N-terminal region of δ2 was indispensable for parallel fiber (PF)-Purkinje cell (PC) synapse formation and/or maintenance, but not for long-term depression (LTD), a form of plasticity in PF-PC synapses. We also found that PTPMEG, a tyrosine phosphatase interacting with the C-terminal region of δ2, dephosphorylated type-2 glutamate receptors in the induction of LTD.