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首页> 外文期刊>The European Journal of Neuroscience >Ca2+-dependent regulation of synaptic delta2 glutamate receptor density in cultured rat Purkinje neurons.
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Ca2+-dependent regulation of synaptic delta2 glutamate receptor density in cultured rat Purkinje neurons.

机译：Ca2 +依赖调节培养的大鼠浦肯野神经元的突触delta2谷氨酸受体密度。

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摘要

The delta2 glutamate receptor (delta2 receptor), which is expressed abundantly at parallel fibre-Purkinje neuron synapses, has an important role in synaptogenesis and synaptic plasticity in the cerebellum. The present study examined the molecular mechanisms regulating synaptic delta2 receptor density. Immunocytochemistry, using two antibodies against the intracellular C-terminal and extracellular N-terminal regions of the delta2 receptor, indicated the reversible redistribution of postsynaptic delta2 receptors in response to either glutamatergic stimulation or enhancement of synaptic activity. The effect of glutamatergic stimulation was completely inhibited by either coapplication of the glutamate receptor antagonist or the removal of extracellular Ca2+ using EGTA and mimicked by selective activation of voltage-gated Ca2+ channels (VGCCs) with KCl, suggesting the significant role of Ca2+ influx in delta2 receptor redistribution. Biochemical examination indicated that a large amount of delta2 receptor protein was internalized following glutamatergic stimulation. These results suggest that the number of synaptic delta2 receptors is controlled by endocytosis in a synaptic activity- and intracellular Ca2+-dependent way, through which synaptogenesis and synaptic plasticity in Purkinje cells might be modulated.
机译：δ2谷氨酸受体（delta2受体）在平行纤维-浦肯野神经元突触中大量表达，在小脑的突触发生和突触可塑性中具有重要作用。本研究检查了调节突触delta2受体密度的分子机制。免疫细胞化学使用两种针对delta2受体胞内C端和胞外N端区域的抗体，表明对谷氨酸能刺激或突触活性增强有反应的突触后delta2受体可逆重新分布。通过联合应用谷氨酸受体拮抗剂或使用EGTA去除细胞外Ca2 +可以完全抑制谷氨酸能刺激的作用，并通过用KCl选择性激活电压门控的Ca2 +通道（VGCC）来模拟，这表明Ca2 +流入在delta2中的重要作用受体再分布。生化检查表明，谷氨酸能刺激后大量的delta2受体蛋白被内在化。这些结果表明，通过内吞作用以突触活性和细胞内Ca 2+依赖性方式控制突触delta 2受体的数量，可以通过其来调节浦肯野细胞中的突触发生和突触可塑性。

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