Macroautophagy/autophagy is implicated in the maintenance of normal neuronal activity through the regulation of synaptic function and plasticity. However, differences in autophagic degradation within different classes of neurons have not been examined. We have recently demonstrated that autophagy plays very different roles in the two closely related principal neurons of the striatum - the spiny projection neurons of the direct (dSPN) and indirect (iSPN) pathways. Behavioral and electrophysiological experiments revealed that the absence of autophagy in either of these SPN pathways produces unique effects on motor learning, dendritic length, and intrinsic excitability. Specifically, autophagy is required for the normal development of synaptic inputs onto dSPNs, while being required for intrinsic excitability in iSPNs. In iSPNs, this occurs through the regulation of the activity of the KCNJ/Kir2 ion channel, and provides a first demonstration of autophagic control of neuronal intrinsic excitability. ABBREVIATIONS ASD: autism spectrum disorders; dSPNs: direct pathway spiny projection neurons; iSPNs: indirect pathway spiny projection neurons; Kir2: inwardly rectifying potassium channel 2.

中文翻译：

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纹状体自噬。

巨自噬/自噬通过调节突触功能和可塑性参与维持正常的神经元活动。但是，尚未检查不同类别神经元内自噬降解的差异。我们最近证明，自噬在纹状体的两个紧密相关的主要神经元中发挥着非常不同的作用-直接（dSPN）和间接（iSPN）途径的多刺投射神经元。行为和电生理实验表明，这些SPN途径中的任何一种都不存在自噬，会对运动学习，树突长度和内在兴奋性产生独特的影响。具体而言，自噬是将突触输入正常发展至dSPN所必需的，而自噬则是iSPN中固有的兴奋性所必需的。在iSPN中，这是通过调节KCNJ / Kir2离子通道的活性而发生的，并首次证明了自噬控制神经元内在兴奋性。缩写ASD：自闭症谱系障碍；dSPNs：直接途径的棘突投射神经元；iSPNs：间接途径的棘突投射神经元；Kir2：向内整流钾离子通道2。