近日美国科学家宣布，在大脑如何对记忆进行编码方面发现了一种新的关键蛋白质在进行大脑记忆的过程中具有重要的作用。
据悉，这是揭示人类记忆编码进程的首次重大发现。美国加州大学科学家肯尼斯-森-科西克（Kenneth S. Kosik）和神经系统科学研究的哈里曼-奇尔（Harriman Chair）表示：这些蛋白质可以建立神经元突触，在我们学习新事物、储存记忆的时候，这些蛋白质建立和加强了大脑中的神经元突触，使得神经元突触对记忆进行编码，从而实现了大脑的记忆能力。
同时，据试验研究表明，这种新蛋白质只有在RNA启动时才会产生。科研人员表示：当诸如想法或者某类刺激的东西进入我们的大脑的时候，我们大脑中的神经突触就被激活了。此时大脑中的一种小RNA将会关闭特定RNA的表达，这就使得这种蛋白质不会随随便便的被产生，也就意味着大脑不会出现记忆错乱。
更有趣的是，当科研人员将提取到得这种关键蛋白质应用到人工培养的神经元中时，实验小鼠的神经元突触也能得到激活。这表明，如果将这种关键蛋白质利用到药物中去，就有可能制造恢复记忆的药物。
据报道，在这次研究实验中，科学家们使用的研究方法之一是从老鼠体内提取活的神经元细胞，然后通过高分辨率的显微镜对其进行观察。这样，科学家们才得以看到神经元突触以及蛋白质制造位置。（生物谷Bioon.com）
生物谷推荐原始出处：
Neuron, Volume 64, Issue 6, 871-884, 24 December 2009 doi:10.1016/j.neuron.2009.11.023
A Coordinated Local Translational Control Point at the Synapse Involving Relief from Silencing and MOV10 Degradation
Sourav Banerjee1, Pierre Neveu1, 2 and Kenneth S. Kosik1, ,
1 Neuroscience Research Institute and Department of Cellular Molecular and Developmental Biology, University of California, Santa Barbara, Santa Barbara, CA 93106, USA
2 Kavli Institute for Theoretical Physics, University of California, Santa Barbara, Santa Barbara, CA 93106, USA
Persistent changes in synaptic strength are locally regulated by both protein degradation and synthesis; however, the coordination of these opposing limbs is poorly understood. Here, we found that the RISC protein MOV10 was present at synapses and was rapidly degraded by the proteasome in an NMDA-receptor-mediated activity-dependent manner. We designed a translational trap to capture those mRNAs whose spatiotemporal translation is regulated by MOV10. When MOV10 was suppressed, a set of mRNAs—including α-CaMKII, Limk1, and the depalmitoylating enzyme lysophospholipase1 (Lypla1)—selectively entered the polysome compartment. We also observed that Lypla1 mRNA is associated with the brain-enriched microRNA miR-138. Using a photoconvertible translation reporter, Kaede, we analyzed the activity-dependent protein synthesis driven by Lypla1 and α-CaMKII 3′UTRs. We established this protein synthesis to be MOV10 and proteasome dependent. These results suggest a unifying picture of a local translational regulatory mechanism during synaptic plasticity.
