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首页> 外文期刊>The European Journal of Neuroscience >Glutamate receptor targeting in the postsynaptic spine involves mechanisms that are independent of myosin Va.
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Glutamate receptor targeting in the postsynaptic spine involves mechanisms that are independent of myosin Va.

机译：谷氨酸受体靶向突触后脊柱涉及独立于肌球蛋白Va的机制。

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Targeting of glutamate receptors (GluRs) to synapses involves rapid movement of intracellular receptors. This occurs in forms of synaptic upregulation of receptors, such as long-term potentiation. Thus, many GluRs are retained in a cytoplasmic pool in dendrites, and are transported to synapses for upregulation, presumably via motor proteins such as myosins travelling along cytoskeletal elements that extend up into the spine. In this ultrastructural immunogold study of the cerebellar cortex, we compared synapses between normal rats/mice and dilute lethal mutant mice. These mutant mice lack myosin Va, which has been implicated in protein trafficking at synapses. The postsynaptic spine in the cerebellum lacks the inositol trisphosphate receptor (IP3R) -laden reticular tubules that are found in normal mice and rats (Takagishi et al., Neurosci. Lett., 1996, 215, 169). Thus, we tested the hypothesis that myosin Va is necessary for transport of GluRs and associated proteins to spine synapses. We found that these spines retain a normal distribution of (i) GluRs (delta 1/2, GluR2/3 and mGluR1alpha), (ii) at least one associated MAGUK (membrane-associated guanylate kinase) protein, (iii) Homer (which interacts with mGluR1alpha and IP3Rs), (iv) the actin cytoskeleton, (v) the reticulum-associated protein BiP, and (vi) the motor-associated protein, dynein light chain. Thus, while myosin Va may maintain the IP3R-laden reticulum in the spine for proper calcium regulation, other mechanisms must be involved in the delivery of GluRs and associated proteins to synapses. Other possible mechanisms include diffusion along the extrasynaptic membrane and delivery via other motors running along the spine's actin cytoskeleton.
机译：将谷氨酸受体（GluRs）靶向突触涉及细胞内受体的快速运动。这以受体的突触上调的形式发生，例如长期增强。因此，许多GluRs保留在树突的细胞质池中，并被转运至突触以进行上调，大概是通过运动蛋白（如肌球蛋白）沿延伸到脊柱的细胞骨架元件行进的。在小脑皮质的超微结构免疫金研究中，我们比较了正常大鼠/小鼠和致死性突变小鼠的突触。这些突变小鼠缺乏肌球蛋白Va，其与突触中的蛋白运输有关。小脑的突触后脊柱缺乏在正常小鼠和大鼠中发现的富含肌醇三磷酸受体（IP3R）的网状小管（Takagishi等人，Neurosci.Lett。，1996，215，169）。因此，我们测试了肌球蛋白Va是将GluRs和相关蛋白转运到脊柱突触所必需的假说。我们发现这些棘突保留（i）GluRs（δ1/2，GluR2 / 3和mGluR1alpha），（ii）至少一种相关的MAGUK（膜相关鸟苷酸激酶），（iii）Homer（与mGluR1alpha和IP3Rs相互作用），（iv）肌动蛋白细胞骨架，（v）与网状蛋白相关的蛋白BiP，和（vi）与运动相关的蛋白，达因轻链。因此，尽管肌球蛋白Va可以维持脊柱中充满IP3R的网状结构以适当调节钙，但在将GluRs和相关蛋白传递到突触中必须涉及其他机制。其他可能的机制包括沿着突触外膜的扩散以及通过其他沿着脊柱肌动蛋白细胞骨架运行的马达的传递。

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