卡羅琳斯卡研究所研究人員發(fā)現(xiàn)了控制大腦產(chǎn)生持久記憶的機(jī)制，該發(fā)現(xiàn)發(fā)表在PNAS雜志上,。研究人員通過給老鼠飲用一種添加過某種化學(xué)物質(zhì)的水，能夠控制老鼠形成長(zhǎng)時(shí)記憶的能力,，這項(xiàng)研究或許對(duì)未來治療阿茲海默癥以及中風(fēng)有重要的意義,。
該課題組最近發(fā)現(xiàn)，通過神經(jīng)元細(xì)胞膜NgR1受體(nogo receptor 1)傳遞的信號(hào)對(duì)大腦形成長(zhǎng)時(shí)記憶過程中有重要作用,。當(dāng)神經(jīng)細(xì)胞被激活后,，NgR1基因關(guān)閉，課題組猜測(cè)NgR1基因失活或許對(duì)形成長(zhǎng)時(shí)記憶有關(guān),。
為了驗(yàn)證該假設(shè),，研究人員建立了攜帶多余NgR1基因片段的老鼠模型,，當(dāng)老鼠基因組中正常的NgR1基因關(guān)閉后,，這一多余片段的NgR1基因仍保持活性狀態(tài)。
研究發(fā)現(xiàn),，在實(shí)驗(yàn)開始的24小時(shí)內(nèi),，這種基因修飾過的老鼠記憶能力仍然正常，但在隨后幾個(gè)月,，通過兩種不同的記憶測(cè)試來看,，這些老鼠在將短時(shí)記憶轉(zhuǎn)化為長(zhǎng)時(shí)記憶時(shí)出現(xiàn)較大的困難。
然后,，研究人員在老鼠飲用水中添加一種無害的化學(xué)物質(zhì),，將這一多余片段的NgR1基因關(guān)閉。當(dāng)該基因關(guān)閉后,，發(fā)現(xiàn)老鼠長(zhǎng)時(shí)記憶的能力逐漸恢復(fù)到正常水平,。
研究人員希望這項(xiàng)發(fā)現(xiàn)能夠應(yīng)用到有記憶障礙的患者中，如阿茲海默癥和中風(fēng)患者,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS November 13, 2009, doi: 10.1073/pnas.0905390106
Nogo receptor 1 regulates formation of lasting memories
Alexandra Karléna, Tobias E. Karlssona,1, Anna Mattssona,1, Karin Lundstr?mera, Simone Codeluppia, Therese M. Phamb, Cristina M. B?ckmanc, Sven Ove ?grena, Elin ?berga, Alexander F. Hoffmanc, Michael A. Sherlingc, Carl R. Lupicac, Barry J. Hofferc, Christian Spengerd, Anna Josephsona, Stefan Brenéb and Lars Olsona,2
aDepartment of Neuroscience, Karolinska Institutet, Retzius v?g 8, 171 77 Stockholm, Sweden;
bDepartment of Neurobiology, Caring Sciences and Society, and
dDepartment of Clinical Science, Intervention and Technology, Karolinska Institutet, 141 86 Stockholm, Sweden; and
cNational Institute on Drug Abuse, National Institutes of Health, 251 Bayview Dr., Baltimore, MD 21224
Formation of lasting memories is believed to rely on structural alterations at the synaptic level. We had found that increased neuronal activity down-regulates Nogo receptor-1 (NgR1) in brain regions linked to memory formation and storage, and postulated this to be required for formation of lasting memories. We now show that mice with inducible overexpression of NgR1 in forebrain neurons have normal long-term potentiation and normal 24-h memory, but severely impaired month-long memory in both passive avoidance and swim maze tests. Blocking transgene expression normalizes these memory impairments. Nogo, Lingo-1, Troy, endogenous NgR1, and BDNF mRNA expression levels were not altered by transgene expression, suggesting that the impaired ability to form lasting memories is directly coupled to inability to down-regulate NgR1. Regulation of NgR1 may therefore serve as a key regulator of memory consolidation. Understanding the molecular underpinnings of synaptic rearrangements that carry lasting memories may facilitate development of treatments for memory dysfunction.
