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PNAS：NgR1受体失活与形成长时记忆有关
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卡罗琳斯卡研究所研究人员发现了控制大脑产生持久记忆的机制，该发现发表在PNAS杂志上。研究人员通过给老鼠饮用一种添加过某种化学物质的水，能够控制老鼠形成长时记忆的能力，这项研究或许对未来治疗阿兹海默症以及中风有重要的意义。
该课题组最近发现，通过神经元细胞膜NgR1受体(nogo receptor 1)传递的信号对大脑形成长时记忆过程中有重要作用。当神经细胞被激活后，NgR1基因关闭，课题组猜测NgR1基因失活或许对形成长时记忆有关。
为了验证该假设，研究人员建立了携带多余NgR1基因片段的老鼠模型，当老鼠基因组中正常的NgR1基因关闭后，这一多余片段的NgR1基因仍保持活性状态。
研究发现，在实验开始的24小时内，这种基因修饰过的老鼠记忆能力仍然正常，但在随后几个月，通过两种不同的记忆测试来看，这些老鼠在将短时记忆转化为长时记忆时出现较大的困难。
然后，研究人员在老鼠饮用水中添加一种无害的化学物质，将这一多余片段的NgR1基因关闭。当该基因关闭后，发现老鼠长时记忆的能力逐渐恢复到正常水平。
研究人员希望这项发现能够应用到有记忆障碍的患者中，如阿兹海默症和中风患者。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
https://m.sciencenet.cn/blog-266677-272125.html
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