英國《自然》雜志刊登報告說，瑞士弗里德里希－米舍研究所等機構研究人員觀察實驗鼠大腦結構變化時發(fā)現(xiàn)，如果實驗鼠進入某個房間后遭到電擊，它就會記住這個遭遇，再進入這個房間時就會表現(xiàn)出恐懼，而在其他相似但不同的房間中卻沒有這種表現(xiàn)。研究發(fā)現(xiàn)，在這個過程中，實驗鼠大腦中相關神經元周圍多出了許多突觸結構。

不過，實驗鼠的記憶準確度只能維持較短的時間，在遭電擊兩個星期后，即使是進入相似的房間，它也會表現(xiàn)出恐懼，這說明被電擊的記憶還在，只是大腦開始把相關環(huán)境混淆了。研究發(fā)現(xiàn)，這時其大腦中相關神經元周圍的突觸結構逐漸消失。

但如果再讓實驗鼠回到zui初遭電擊的房間，其相關突觸結構會重新建立，記憶再次變得準確，再進入其他房間也不再表現(xiàn)出恐懼。研究人員據(jù)此認為，突觸結構在大腦記憶中起著確定事件背景、保證記憶準確度的作用。

原文出處：

Nature 　doi:10.1038/nature09946

Sarah Ruediger,1, 3 Claudia Vittori,1, 2, 3 Ewa Bednarek,1 Chris 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.