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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Transient global ischemia enhances phosphorylation of the GluR1 subunit of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor in the hippocampal CA1 region in rats.
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Transient global ischemia enhances phosphorylation of the GluR1 subunit of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor in the hippocampal CA1 region in rats.

机译:短暂性全脑缺血可增强大鼠海马CA1区中α-氨基-3-羟基-5-甲基异恶唑-4-丙酸酯受体GluR1亚基的磷酸化。

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摘要

Phosphorylation of the GluR1 subunit of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptor has been implicated in the regulation of the receptor channel. We investigated the effects of transient global ischemia in rats on phosphorylation of the GluR1 subunit in the hippocampal CA1 and CA3/dentate gyrus. Transient ischemia induced an increase in the phosphorylation of GluR1 at Ser831 in the CA1 at 1 h of reperfusion. In contrast, the phosphorylation of Ser845 in neither region was affected by the ischemia. The amounts of calcium/calmodulin-dependent kinase (CaMKII) and its activated form, but not cAMP-dependent protein kinase subunits, were increased in a crude membrane fraction after ischemia. The results suggest that an activated CaMKII may phosphorylate Ser831 of GluR1 and a consequent phosphorylation of GluR1 may be related to pathogenic events occurring in the vulnerable subfield of the hippocampus after transient global ischemia.
机译:α-氨基-3-羟基-5-甲基异恶唑-4-丙酸酯受体的GluR1亚基的磷酸化与受体通道的调节有关。我们调查了大鼠短暂性全脑缺血对海马CA1和CA3 /齿状回中GluR1亚基磷酸化的影响。短暂性脑缺血导致再灌注1 h CA1中Ser831的GluR1磷酸化增加。相反,在两个区域中,Ser845的磷酸化均不受缺血影响。缺血后,粗膜部分的钙/钙调蛋白依赖性激酶(CaMKII)及其激活形式(而不是cAMP依赖性蛋白激酶亚单位)的数量增加。结果表明,活化的CaMKII可能使GluR1的Ser831磷酸化,因此,GluR1的磷酸化可能与短暂性整体缺血后海马脆弱亚区域中发生的致病事件有关。

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