经常把朋友的名字张冠李戴，或是把事情弄混？这也许是因为你大脑中神经元之间的突触结构正在经历生生灭灭的变化。一项最新研究显示，这种变化会使得记忆准确度随之改变，相关成果或许可用于治疗一些与记忆有关的疾病。
英国《自然》杂志网站刊登报告说，瑞士弗里德里希－米舍研究所等机构研究人员观察实验鼠大脑结构变化时发现，如果实验鼠进入某个房间后遭到电击，它就会记住这个遭遇，再进入这个房间时就会表现出恐惧，而在其他相似但不同的房间中却没有这种表现。研究发现，在这个过程中，实验鼠大脑中相关神经元周围多出了许多突触结构。
不过，实验鼠的记忆准确度只能维持较短的时间，在遭电击两个星期后，即使是进入相似的房间，它也会表现出恐惧，这说明被电击的记忆还在，只是大脑开始把相关环境混淆了。研究发现，这时其大脑中相关神经元周围的突触结构逐渐消失。
但如果再让实验鼠回到最初遭电击的房间，其相关突触结构会重新建立，记忆再次变得准确，再进入其他房间也不再表现出恐惧。研究人员据此认为，突触结构在大脑记忆中起着确定事件背景、保证记忆准确度的作用。（生物谷Bioon.com）
生物谷推荐原文出处：
Nature doi:10.1038/nature09946
Learning-related feedforward inhibitory connectivity growth required for memory precision
Sarah Ruediger,1, 3 Claudia Vittori,1, 2, 3 Ewa Bednarek,1 Christel Genoud,1 Piergiorgio Strata,2 Benedetto Sacchetti2 & Pico Caroni1
In the adult brain, new synapses are formed and pre-existing ones are lost, but the function of this structural plasticity has remained unclear1, 2, 3, 4, 5. Learning of new skills is correlated with formation of new synapses6, 7, 8. These may directly encode new memories, but they may also have more general roles in memory encoding and retrieval processes2. Here we investigated how mossy fibre terminal complexes at the entry of hippocampal and cerebellar circuits rearrange upon learning in mice, and what is the functional role of the rearrangements. We show that one-trial and incremental learning lead to robust, circuit-specific, long-lasting and reversible increases in the numbers of filopodial synapses onto fast-spiking interneurons that trigger feedforward inhibition. The increase in feedforward inhibition connectivity involved a majority of the presynaptic terminals, restricted the numbers of c-Fos-expressing postsynaptic neurons at memory retrieval, and correlated temporally with the quality of the memory. We then show that for contextual fear conditioning and Morris water maze learning, increased feedforward inhibition connectivity by hippocampal mossy fibres has a critical role for the precision of the memory and the learned behaviour. In the absence of mossy fibre long-term potentiation in Rab3a?/? mice9, c-Fos ensemble reorganization and feedforward inhibition growth were both absent in CA3 upon learning, and the memory was imprecise. By contrast, in the absence of adducin 2 (Add2; also known as β-adducin)10 c-Fos reorganization was normal, but feedforward inhibition growth was abolished. In parallel, c-Fos ensembles in CA3 were greatly enlarged, and the memory was imprecise. Feedforward inhibition growth and memory precision were both rescued by re-expression of Add2 specifically in hippocampal mossy fibres. These results establish a causal relationship between learning-related increases in the numbers of defined synapses and the precision of learning and memory in the adult. The results further relate plasticity and feedforward inhibition growth at hippocampal mossy fibres to the precision of hippocampus-dependent memories.
