可能所有人都希望擦除腦海中痛苦的記憶，如今科學(xué)家或許可以實(shí)現這種美好的愿望。美國加利福尼亞大學(xué)科學(xué)家近日宣稱(chēng)，他們已經(jīng)找到一種可能從腦海中刪除創(chuàng )傷的方法，這種方法讓忘記痛苦回憶成為一種可能。

科學(xué)家們已經(jīng)找到了一種被稱(chēng)為PKM的蛋白質(zhì)與煩惱回憶之間的聯(lián)系，他們的研究成果發(fā)表于《神經(jīng)系統科學(xué)》雜志上。對于戰爭老兵、暴力犯罪受害者等人來(lái)說(shuō)，這一發(fā)現具有非常重要的意義。加利福尼亞大學(xué)科學(xué)家大衛-格蘭茲曼是該項研究的主要負責人。格蘭茲曼表示，“我認為，我們有一天可以改變記憶，從而抹除我們大腦中的創(chuàng )傷。當然，這一天并不是在最近。但是，我認為我們能夠深入大腦，識別創(chuàng )傷經(jīng)歷的記憶位置，并試圖將其淡化。”

格蘭茲曼是一位細胞神經(jīng)學(xué)家。他的研究團隊報告稱(chēng)，他們已經(jīng)抹除了(至少已實(shí)質(zhì)弱化)海蝸牛體內以及有蓋培養皿中神經(jīng)元的長(cháng)期記憶。研究人員表示，他們對長(cháng)期記憶的細胞生物學(xué)的研究已經(jīng)取得了重要進(jìn)展。

研究人員發(fā)現，海蝸牛體內負責感應的長(cháng)期記憶可以通過(guò)抑制PKM蛋白質(zhì)的活動(dòng)而被逐漸抹除，PKM蛋白質(zhì)是一種與記憶相關(guān)的蛋白質(zhì)。科學(xué)家表示，這項研究成果還可用于戒毒、治療阿爾茨海默病以及其他長(cháng)期記憶混亂疾病。

科學(xué)家之所以選擇海蝸牛體內的PKM，是因為海蝸牛擁有簡(jiǎn)單的學(xué)習形式和簡(jiǎn)單的神經(jīng)系統。通過(guò)研究，科學(xué)家可以深入地了解PKM的活動(dòng)究竟是如何維持長(cháng)期記憶的。此前，科學(xué)家們對這一過(guò)程知之甚少。研究人員對一種簡(jiǎn)單的記憶進(jìn)行了研究。如果海蝸牛被捕食者攻擊，攻擊會(huì )提高它們對環(huán)境的敏感度。這是一種最基本的學(xué)習形式，也是生存的必要技能。

最終，科學(xué)家們成功地抹除了海蝸牛和有蓋培養皿中神經(jīng)元的長(cháng)期記憶。科學(xué)家首次證明，長(cháng)期記憶可以在兩個(gè)神經(jīng)元之間抹除。

原文出處：

Journal of Neuroscience, 2011; 31 (17): 6421 DOI: 10.1523/JNEUROSCI.4744-10.2011

Protein Kinase M Maintains Long-Term Sensitization and Long-Term Facilitation in Aplysia

D. Cai, K. Pearce, S. Chen, D. L. Glanzman

Abstract

How the brain maintains long-term memories is one of the major outstanding questions in modern neuroscience. Evidence from mammalian studies indicates that activity of a protein kinase C (PKC) isoform, protein kinase Mζ (PKMζ), plays a critical role in the maintenance of long-term memory. But the range of memories whose persistence depends on PKMζ, and the mechanisms that underlie the effect of PKMζ on long-term memory, remain obscure. Recently, a PKM isoform, known as PKM Apl III, was cloned from the nervous system of Aplysia. Here, we tested whether PKM Apl III plays a critical role in long-term memory maintenance in Aplysia. Intrahemocoel injections of the pseudosubstrate inhibitory peptide ZIP (ζ inhibitory peptide) or the PKC inhibitor chelerythrine erased the memory for long-term sensitization (LTS) of the siphon-withdrawal reflex (SWR) as late as 7 d after training. In addition, both PKM inhibitors disrupted the maintenance of long-term (≥24 h) facilitation (LTF) of the sensorimotor synapse, a form of synaptic plasticity previously shown to mediate LTS of the SWR. Together with previous results (Bougie et al., 2009), our results support the idea that long-term memory in Aplysia is maintained via a positive-feedback loop involving PKM Apl III-dependent protein phosphorylation. The present data extend the known role of PKM in memory maintenance to a simple and well studied type of long-term learning. Furthermore, the demonstration that PKM activity underlies the persistence of LTF of the Aplysia sensorimotor synapse, a form of synaptic plasticity amenable to rigorous cellular and molecular **yses, should facilitate efforts to understand how PKM activity maintains memory.