The delta2 'ionotropic' glutamate receptor functions as a non-ionotropic receptor to control cerebellar synaptic plasticity.
The delta2 'ionotropic' glutamate receptor functions as a non-ionotropic receptor to control cerebellar synaptic plasticity.
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发表时间：
2007
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通讯作者：
W. Kakegawa;K. Kohda;M. Yuzaki
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作者：
W. Kakegawa;K. Kohda;M. Yuzaki
delta 2谷氨酸受体（GluRdelta 2）属于离子型谷氨酸受体（iGluR）家族，并且在小脑长时程抑制（LTD）的诱导中起关键作用，所述LTD是运动学习基础的突触可塑性的一种形式。然而，GluRdelta 2调节小脑LTD的机制仍然难以捉摸。因为在lurcher小鼠中发生的突变引起连续的GluRdelta 2通道活性，该活性可以被1-萘基乙酰精胺（NASP）（Ca（2+）-可渗透iGluRs的通道阻断剂）消除，所以GluRdelta 2被认为起离子通道的作用。在这里，我们介绍了一个突变体GluRdelta 2转基因，其中假定的通道孔被破坏，到GluRdelta 2空浦肯野细胞使用病毒载体。令人惊讶的是，与野生型GluRdelta 2转基因的作用相似，突变型GluRdelta 2完全挽救了GluRdelta 2缺失小鼠中废除的LTD。此外，NASP没有阻断LTD诱导野生型小脑切片。这些结果表明，GluRdelta 2，iGluR家族的成员，不作为一个通道，在调节LTD诱导。
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.