Raab-Graham Kimberly F, Haddick Patrick C G, Jan Yuh Nung, Jan Lily Yeh
Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94158, USA.
Science. 2006 Oct 6;314(5796):144-8. doi: 10.1126/science.1131693.
Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-d-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.
雷帕霉素的哺乳动物靶点（mTOR）与突触可塑性和树突中的局部翻译有关。我们发现，mTOR抑制剂雷帕霉素可增加海马神经元中Kv1.1电压门控钾通道蛋白的含量，并促进Kv1.1在树突上的表面表达，而不改变其在轴突上的表达。此外，在树突中检测到内源性Kv1.1 mRNA。使用与光转换荧光蛋白Kaede融合的Kv1.1作为局部合成的报告基因，我们观察到在抑制mTOR或N-甲基-D-天冬氨酸（NMDA）谷氨酸受体后，树突中Kv1.1的合成。因此，突触兴奋可能通过减少树突Kv1通道的局部合成而导致其局部抑制。
