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首页> 外文期刊>The European Journal of Neuroscience >Induction and expression of GluA1 (GluR-A)-independent LTP in the hippocampus.
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Induction and expression of GluA1 (GluR-A)-independent LTP in the hippocampus.

机译：海马中不依赖GluA1（GluR-A）的LTP的诱导和表达。

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摘要

Long-term potentiation (LTP) at hippocampal CA3-CA1 synapses is thought to be mediated, at least in part, by an increase in the postsynaptic surface expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptors induced by N-methyl-d-aspartate (NMDA) receptor activation. While this process was originally attributed to the regulated synaptic insertion of GluA1 (GluR-A) subunit-containing AMPA receptors, recent evidence suggests that regulated synaptic trafficking of GluA2 subunits might also contribute to one or several phases of potentiation. However, it has so far been difficult to separate these two mechanisms experimentally. Here we used genetically modified mice lacking the GluA1 subunit (Gria1(-/-) mice) to investigate GluA1-independent mechanisms of LTP at CA3-CA1 synapses in transverse hippocampal slices. An extracellular, paired theta-burst stimulation paradigm induced a robust GluA1-independent form of LTP lacking the early, rapidly decaying component characteristic of LTP in wild-type mice. This GluA1-independent form of LTP was attenuated by inhibitors of neuronal nitric oxide synthase and protein kinase C (PKC), two enzymes known to regulate GluA2 surface expression. Furthermore, the induction of GluA1-independent potentiation required the activation of GluN2B (NR2B) subunit-containing NMDA receptors. Our findings support and extend the evidence that LTP at hippocampal CA3-CA1 synapses comprises a rapidly decaying, GluA1-dependent component and a more sustained, GluA1-independent component, induced and expressed via a separate mechanism involving GluN2B-containing NMDA receptors, neuronal nitric oxide synthase and PKC.
机译：据认为，海马CA3-CA1突触的长期增强（LTP）至少部分地由α-氨基-3-羟基-5-甲基-5-甲基-4-异恶唑丙酸的突触后表面表达的增加来介导。 N-甲基-d-天冬氨酸（NMDA）受体激活诱导的（AMPA）受体。虽然此过程最初归因于GluA1（GluR-A）亚基的AMPA受体的突触插入的调节，但最近的证据表明，GluA2亚基的突触运输的调节也可能有助于一个或几个增强阶段。但是，到目前为止，很难通过实验将这两种机制分开。在这里，我们使用了缺少GluA1亚基的转基因小鼠（Gria1（-/-）小鼠）来研究横纹海马切片中CA3-CA1突触处LTP的GluA1依赖性机制。细胞外，成对的theta-burst刺激范例诱导了LTP的一种健壮的GluA1独立形式，而在野生型小鼠中缺少LTP的早期，快速衰减的成分特征。 LTP的这种GluA1独立形式被神经元一氧化氮合酶和蛋白激酶C（PKC）的抑制剂所减弱，这两种酶已知可调节GluA2表面表达。此外，诱导GluA1独立增强需要激活包含GluN2B（NR2B）亚基的NMDA受体。我们的发现支持并扩展了证据，即海马CA3-CA1突触处的LTP包括快速衰减的GluA1依赖性成分和更持久的GluA1依赖性成分，其通过涉及包含GluN2B的NMDA受体，神经元一氧化氮的单独机制诱导和表达。氧化物合酶和PKC。

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