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首页> 外文期刊>Neuron >Cerebellar long-term depression requires PKC-regulated interactions between GluR2/3 and PDZ domain-containing proteins.
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Cerebellar long-term depression requires PKC-regulated interactions between GluR2/3 and PDZ domain-containing proteins.

机译：小脑的长期抑郁症需要GluR2 / 3与含PDZ域的蛋白质之间的PKC调控相互作用。

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摘要

Cerebellar LTD requires activation of PKC and is expressed, at least in part, as postsynaptic AMPA receptor internalization. Recently, it was shown that AMPA receptor internalization requires clathrin-mediated endocytosis and depends upon the carboxy-terminal region of GluR2/3. Phosphorylation of Ser-880 in this region by PKC differentially regulates the binding of the PDZ domain-containing proteins GRIP/ABP and PICK1. Peptides, corresponding to the phosphorylated and dephosphorylated GluR2 carboxy-terminal PDZ binding motif, were perfused in cerebellar Purkinje cells grown in culture. Both the dephospho form (which blocks binding of GRIP/ABP and PICK1) and the phospho form (which selectively blocks PICK1) attenuated LTD induction by glutamate/depolarization pairing, as did antibodies directed against the PDZ domain of PICK1. These findings indicate that expression of cerebellar LTD requires PKC-regulated interactions between the carboxy-terminal of GluR2/3 and PDZ domain-containing proteins.
机译：小脑LTD需要激活PKC，并至少部分以突触后AMPA受体内部化的形式表达。最近，已经表明AMPA受体内在化需要网格蛋白介导的内吞作用，并且依赖于GluR2 / 3的羧基末端区域。 PKC使该区域的Ser-880磷酸化差异调节含PDZ域的蛋白质GRIP / ABP和PICK1的结合。在培养物中生长的小脑浦肯野细胞中灌注相应于磷酸化和脱磷酸化的GluR2羧基末端PDZ结合基序的肽。脱磷酸形式（阻止GRIP / ABP和PICK1的结合）和磷酸形式（选择性地阻止PICK1）都通过谷氨酸/去极化配对减弱了LTD的诱导，抗PICK1 PDZ域的抗体也是如此。这些发现表明，小脑LTD的表达需要GluR2 / 3的羧基末端与含PDZ域的蛋白质之间的PKC调控相互作用。

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