Schmitt W B, Sprengel R, Mack V, Draft R W, Seeburg P H, Deacon R M J, Rawlins J N P, Bannerman D M
Department of Experimental Psychology, University of Oxford, South Parks Road, Oxford, OX1 3UD, UK.
Nat Neurosci. 2005 Mar;8(3):270-2. doi: 10.1038/nn1412. Epub 2005 Feb 20.
Gene-targeted mice lacking the AMPA receptor subunit GluR-A (also called GluR1 encoded by the gene Gria1,) have deficits in hippocampal CA3-CA1 long-term potentiation (LTP) and have profoundly impaired hippocampus-dependent spatial working memory (SWM) tasks, although their spatial reference memory remains normal. Here we show that forebrain-localized expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, paralleling its rescue of CA3-CA1 LTP. This provides powerful new evidence linking hippocampal GluR-A-dependent synaptic plasticity to rapid, flexible memory processing.
缺乏AMPA受体亚基GluR - A(也称为由基因Gria1编码的GluR1)的基因靶向小鼠,在海马CA3 - CA1长时程增强(LTP)方面存在缺陷,并且在依赖海马的空间工作记忆(SWM)任务中表现出严重受损,尽管它们的空间参考记忆保持正常。在这里,我们表明,在GluR - A缺陷小鼠中,前脑定位表达的绿色荧光蛋白标记的GluR - A亚基可挽救SWM,这与其对CA3 - CA1 LTP的挽救情况相似。这为将海马中依赖GluR - A的突触可塑性与快速、灵活的记忆处理联系起来提供了有力的新证据。