美國佛羅里達大學(xué)斯克利普斯研究所的科學(xué)家發(fā)現(xiàn)了一條對長期記憶形成起關(guān)鍵作用的機制,。這個發(fā)現(xiàn)不僅闡明了記憶是如何形成的，也有助于發(fā)展記憶障礙性疾病治療的新途徑,。研究結(jié)果發(fā)表在《Neuron》雜志上,。
在研究中科學(xué)家們發(fā)現(xiàn)了一個記憶形成的主要驅(qū)動子myosin II，它是細胞移動和生長的一個關(guān)鍵動力蛋白,。“我們第一次證實了myosin II在記憶形成中發(fā)揮主要作用,，我們也接近于確定導(dǎo)致這個大腦動力蛋白激活的信號途徑。”佛羅里達大學(xué)斯克利普斯研究所該項研究的負責(zé)人Gavin Rumbaugh說：“一旦我們找到關(guān)鍵的信號途徑,，我們將開始致力開發(fā)有效的治療方法幫助那些存在認知障礙的人們比如阿爾茲海默病的患者恢復(fù)記憶,。”
Rumbaugh和他的同事們證實myosin II在記憶形成復(fù)雜過程中發(fā)揮調(diào)控作用。myosin II與長時程增強效應(yīng)啟動相關(guān),啟動長時程增強效可增強神經(jīng)元之間的信號傳遞,，穩(wěn)定神經(jīng)元突觸可塑性以及重組神經(jīng)元F-actin,。
對大腦的刺激激活了了這些myosin動力蛋白，啟動了F-actin的生長最后穩(wěn)定了長時程增強效應(yīng),。”Rumbaugh說：“大腦記錄我們經(jīng)歷的過程就是突觸生長和強化的過程,。我們現(xiàn)在了解到突觸間的物質(zhì)使得我們的生命經(jīng)歷得以儲存下來。”
他在研究中補充說明了F-actin的作用,。長時程增強效應(yīng)依賴于突觸結(jié)構(gòu)的改變表明myosinII啟動的動態(tài)重組是信息編碼的早期步驟。
“許多并行大腦處理過程被激活參與信息儲存,。如果他們中的任何一個被破壞,，信息就會失去穩(wěn)定，記憶就會喪失,。myosinII是這個過程的關(guān)鍵調(diào)控因子,，如果你能通過藥物控制myosin II，你就能隨意有效地控制記憶,。”Rumbaugh說,。（生物谷Bioon.com）
生物谷推薦原文出處：
Neuron doi：10.1016/j.neuron.2010.07.016
Myosin IIb Regulates Actin Dynamics during Synaptic Plasticity and Memory Formation
Christopher S. Rex, Cristin F. Gavin, Maria D. Rubio, Eniko A. Kramar, Lulu Y. Chen, Yousheng Jia, Richard L. Huganir, Nicholas Muzyczka, Christine M. Gall, Courtney A. Miller, Gary Lynch, Gavin Rumbaugh
Highlights
Defines a mechanical process controlling F-actin reorganization at synapses
Myosin II motor activity is engaged by LTP induction
Myosin II activity produces de novo actin filaments at synapses that maintain LTP
Myosin II activity regulates actin polymerization that supports memory formation
Summary
Reorganization of the actin cytoskeleton is essential for synaptic plasticity and memory formation. Presently, the mechanisms that trigger actin dynamics during these brain processes are poorly understood. In this study, we show that myosin II motor activity is downstream of LTP induction and is necessary for the emergence of specialized actin structures that stabilize an early phase of LTP. We also demonstrate that myosin II activity contributes importantly to an actin-dependent process that underlies memory consolidation. Pharmacological treatments that promote actin polymerization reversed the effects of a myosin II inhibitor on LTP and memory. We conclude that myosin II motors regulate plasticity by imparting mechanical forces onto the spine actin cytoskeleton in response to synaptic stimulation. These cytoskeletal forces trigger the emergence of actin structures that stabilize synaptic plasticity. Our studies provide a mechanical framework for understanding cytoskeletal dynamics associated with synaptic plasticity and memory formation.
