近日美國科學(xué)家宣布,，在大腦如何對(duì)記憶進(jìn)行編碼方面發(fā)現(xiàn)了一種新的關(guān)鍵蛋白質(zhì)在進(jìn)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(jìn)程的首次重大發(fā)現(xiàn),。美國加州大學(xué)科學(xué)家肯尼斯-森-科西克（Kenneth S. Kosik）和神經(jīng)系統(tǒng)科學(xué)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(xué)習(xí)新事物、儲(chǔ)存記憶的時(shí)候,，這些蛋白質(zhì)建立和加強(qiáng)了大腦中的神經(jīng)元突觸,，使得神經(jīng)元突觸對(duì)記憶進(jìn)行編碼，從而實(shí)現(xiàn)了大腦的記憶能力,。
同時(shí),，據(jù)試驗(yàn)研究表明，這種新蛋白質(zhì)只有在RNA啟動(dòng)時(shí)才會(huì)產(chǎn)生?？蒲腥藛T表示：當(dāng)諸如想法或者某類刺激的東西進(jìn)入我們的大腦的時(shí)候,，我們大腦中的神經(jīng)突觸就被激活了。此時(shí)大腦中的一種小RNA將會(huì)關(guān)閉特定RNA的表達(dá),，這就使得這種蛋白質(zhì)不會(huì)隨隨便便的被產(chǎn)生,，也就意味著大腦不會(huì)出現(xiàn)記憶錯(cuò)亂。
更有趣的是,，當(dāng)科研人員將提取到得這種關(guān)鍵蛋白質(zhì)應(yīng)用到人工培養(yǎng)的神經(jīng)元中時(shí),，實(shí)驗(yàn)小鼠的神經(jīng)元突觸也能得到激活。這表明,，如果將這種關(guān)鍵蛋白質(zhì)利用到藥物中去,，就有可能制造恢復(fù)記憶的藥物。
據(jù)報(bào)道,，在這次研究實(shí)驗(yàn)中,，科學(xué)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(xì)胞，然后通過高分辨率的顯微鏡對(duì)其進(jìn)行觀察,。這樣,，科學(xué)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.
