歐盟第七研發(fā)框架計劃（FP7）資助290萬歐元，由丹麥,、西班牙和瑞士科學家組成的研究團隊,，在分子和細胞學研究方面取得重要進展，首次發(fā)現(xiàn)提高大腦認知功能的機理,。該發(fā)現(xiàn)對治療老年癡呆癥,、孤獨癥和各種精神失調(diào)疾病具有潛力，研究結果在最新一期的《公共科學圖書館生物學》PLoS Biology雜志上發(fā)表,。
大腦中連接神經(jīng)元的突融,，對人類的認知功能起著舉足輕重的關鍵作用，尤其是控制大腦認知功能活力的突融模式,。嬰兒出生時大腦神經(jīng)元的突融連接并不是固定的,，但突融連接對神經(jīng)元強度和活力的反應明顯。神經(jīng)元的突融連接是動態(tài)的,，并持續(xù)改變著神經(jīng)元的強度和特性,。這一過程在生物學上被稱為突融可塑性（Synaptic Plasticity），突融可塑性形成大腦學習和記憶的細胞基礎,。研究團隊進行的科學探索證實,，人為地操作突融可塑性可以提高大腦的認知功能。
科研人員通過采集來自細胞到細胞信息聯(lián)絡的神經(jīng)元蛋白被稱作縮氨酸肽（Peptide）上的一枚小蛋白片斷,，制作成一枚更大的塑料狀（Plastic-like）突融,，新生成的突融（FGL）引發(fā)神經(jīng)細胞的連鎖反應，為突融可塑性提供了便利。FGL引起新神經(jīng)傳遞素受體進入大腦海馬（Hippocampus）區(qū)域的突融,，從而對增加學習和記憶的多種方式產(chǎn)生積極作用,，成為提高大腦認知功能和醫(yī)治精神紊亂的有效手段。（生物谷Bioon.com）
doi:10.1371/journal.pbio.1001262
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Facilitation of AMPA Receptor Synaptic Delivery as a Molecular Mechanism for Cognitive Enhancement
Shira Knafo1,2#*, César Venero3#*, Cristina Sánchez-Puelles1, Inmaculada Pereda-Peréz3, Ana Franco4, Carmen Sandi5, Luz M. Suárez2,6, José M. Solís6, Lidia Alonso-Nanclares2, Eduardo D. Martín7, Paula Merino-Serrais2, Erika Borcel3, Shizhong Li8, Yongshuo Chen8, Juncal Gonzalez-Soriano9, Vladimir Berezin8, Elisabeth Bock8, Javier DeFelipe2, José A. Esteban1*
Cell adhesion molecules and downstream growth factor-dependent signaling are critical for brain development and synaptic plasticity, and they have been linked to cognitive function in adult animals. We have previously developed a mimetic peptide (FGL) from the neural cell adhesion molecule (NCAM) that enhances spatial learning and memory in rats. We have now investigated the cellular and molecular basis of this cognitive enhancement, using biochemical, morphological, electrophysiological, and behavioral analyses. We have found that FGL triggers a long-lasting enhancement of synaptic transmission in hippocampal CA1 neurons. This effect is mediated by a facilitated synaptic delivery of AMPA receptors, which is accompanied by enhanced NMDA receptor-dependent long-term potentiation (LTP). Both LTP and cognitive enhancement are mediated by an initial PKC activation, which is followed by persistent CaMKII activation. These results provide a mechanistic link between facilitation of AMPA receptor synaptic delivery and improved hippocampal-dependent learning, induced by a pharmacological cognitive enhancer.
