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首页> 外文期刊>Neuron >Insulin receptor signaling regulates synapse number, dendritic plasticity, and circuit function in vivo.
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Insulin receptor signaling regulates synapse number, dendritic plasticity, and circuit function in vivo.

机译：胰岛素受体信号传导在体内调节突触数量，树突可塑性和电路功能。

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摘要

Insulin receptor signaling has been postulated to play a role in synaptic plasticity; however, the function of the insulin receptor in CNS is not clear. To test whether insulin receptor signaling affects visual system function, we recorded light-evoked responses in optic tectal neurons in living Xenopus tadpoles. Tectal neurons transfected with dominant-negative insulin receptor (dnIR), which reduces insulin receptor phosphorylation, or morpholino against insulin receptor, which reduces total insulin receptor protein level, have significantly smaller light-evoked responses than controls. dnIR-expressing neurons have reduced synapse density as assessed by EM, decreased AMPA mEPSC frequency, and altered experience-dependent dendritic arbor structural plasticity, although synaptic vesicle release probability, assessed by paired-pulse responses, synapse maturation, assessed by AMPA/NMDA ratio and ultrastructural criteria, are unaffected by dnIR expression. These data indicate that insulin receptor signaling regulates circuit function and plasticity by controlling synapse density.
机译：胰岛素受体信号传导被认为在突触可塑性中发挥作用。然而，胰岛素受体在中枢神经系统中的功能尚不清楚。为了测试胰岛素受体信号传导是否影响视觉系统功能，我们在活着的爪蟾的视神经顶盖神经元中记录了光诱发的反应。用显性负性胰岛素受体（dnIR）转染的直肠神经元可减少胰岛素受体的磷酸化，或针对胰岛素受体的吗啉代可降低总胰岛素受体蛋白的水平，其光诱发的反应明显小于对照。通过EM评估，表达dnIR的神经元具有降低的突触密度，降低的AMPA mEPSC频率并改变了经验依赖性的树突状乔木结构可塑性，尽管通过成对脉冲响应评估的突触小泡释放概率，通过AMPA / NMDA比评估的突触成熟和超微结构标准不受dnIR表达的影响。这些数据表明，胰岛素受体信号传导通过控制突触密度来调节电路功能和可塑性。

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