Insulin-like growth factor I potentiates kainate receptors through a phosphatidylinositol 3-kinase dependent pathway
Insulin-like growth factor I potentiates kainate receptors through a phosphatidylinositol 3-kinase dependent pathway
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DOI：
10.1097/00001756-200105080-00047
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发表时间：
2001-05-08
期刊：
影响因子：
1.7
通讯作者：
Torres-Aleman, I
中科院分区：
文献类型：
--
作者：
de la Vega, AG;Buño, W;Torres-Aleman, I
神经营养因子通过调节膜离子通道和神经递质受体等机制调节突触可塑性。最近的研究表明，胰岛素样生长因子I(IGF-I)可以抑制AMPA介导的电流，而不影响NMDA受体的功能。我们现在报道，IGF-I显著增强表达功能性红藻氨酸介导的电流的年轻小脑颗粒神经元上的红藻氨酸偏爱离子型谷氨酸受体，但不是AMPA介导的电流。IGF-I对海人藻酸反应的增强作用可被磷脂酰肌醇3-激酶(PI3K)抑制剂Wortmannin阻断，这表明该激酶在IGF-I的作用中发挥了作用。这些结果强化了离子亲性谷氨酸受体的调制参与了IGF-I对神经元可塑性的调节作用的观点。《神经报告》12：1293-1296(C)2001 Lippincott Williams&Wilkins.
Neurotrophic factors modulate synaptic plasticity through mechanisms that include regulation of membrane ion channels and neurotransmitter receptors. Recently, it was shown that insulin-like growth factor I (IGF-I) induces depression of AMPA-mediated currents without affecting NMDA-receptor function in neurons. We now report that IGF-I markedly potentiates the kainate-preferring ionotropic glutamate receptor in young cerebellar granule neurons expressing functional kainate-, but not AMPA-mediated currents. Potentiation of kainate responses by IGF-I is blocked by wortmannin, a phosphatidylinositol 3-kinase (PI3K) inhibitor, indicating a role for this kinase in the effect of IGF-I. These results reinforce the notion that modulation of ionotropic glutamate receptors are involved in the regulatory actions of IGF-I on neuronal plasticity. NeuroReport 12:1293-1296 (C) 2001 Lippincott Williams & Wilkins.