近日美國科學家宣布,，在大腦如何對記憶進行編碼方面發(fā)現(xiàn)了一種新的關鍵蛋白質(zhì)在進行大腦記憶的過程中具有重要的作用,。
據(jù)悉,，這是揭示人類記憶編碼進程的首次重大發(fā)現(xiàn)。美國加州大學科學家肯尼斯-森-科西克（Kenneth S. Kosik）和神經(jīng)系統(tǒng)科學研究的哈里曼-奇爾（Harriman Chair）表示：這些蛋白質(zhì)可以建立神經(jīng)元突觸,，在我們學習新事物,、儲存記憶的時候，這些蛋白質(zhì)建立和加強了大腦中的神經(jīng)元突觸,，使得神經(jīng)元突觸對記憶進行編碼,，從而實現(xiàn)了大腦的記憶能力。
同時,，據(jù)試驗研究表明,，這種新蛋白質(zhì)只有在RNA啟動時才會產(chǎn)生?？蒲腥藛T表示：當諸如想法或者某類刺激的東西進入我們的大腦的時候,，我們大腦中的神經(jīng)突觸就被激活了。此時大腦中的一種小RNA將會關閉特定RNA的表達,，這就使得這種蛋白質(zhì)不會隨隨便便的被產(chǎn)生,，也就意味著大腦不會出現(xiàn)記憶錯亂。
更有趣的是,，當科研人員將提取到得這種關鍵蛋白質(zhì)應用到人工培養(yǎng)的神經(jīng)元中時,，實驗小鼠的神經(jīng)元突觸也能得到激活。這表明,，如果將這種關鍵蛋白質(zhì)利用到藥物中去,，就有可能制造恢復記憶的藥物。
據(jù)報道,，在這次研究實驗中，科學家們使用的研究方法之一是從老鼠體內(nèi)提取活的神經(jīng)元細胞,，然后通過高分辨率的顯微鏡對其進行觀察,。這樣，科學家們才得以看到神經(jīng)元突觸以及蛋白質(zhì)制造位置,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
