老鼠脑部植入電極可恢復和增強記憶
配圖：美國科學家們在小鼠身上成功實驗了一種能夠增強記憶、彌補記憶力不足的植入設備，以后有望獲得能夠緩解癡呆等腦補損傷的“人工神經器官”。
領導該實驗的南加州大學科學家西奧多·伯格。
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（JGospel 2011年6月23日）據《紐約時報》報導，美國科學家們在小鼠身上成功實驗了一種能夠增強記憶、彌補記憶力不足的植入設備，不久的將來，醫學界有望獲得能夠緩解癡呆、中風和其它腦補損傷的“人工神經器官”。
“讀心”設備可以讓人只通過思考就操縱儀器，一月份美國科學家將思想植入猴腦，讓猴子“學懂”並分辨出不同的物體就是個很好的例子。現在這個實驗也是同一原理，只是所讀取的“思想”不同，而是將小鼠自己的“思想”在腦中“重播”，結果就是記憶得到了提高。
領導該實驗的南加州大學（University of Southern California，USC）科學家西奧多·伯格（Theodore Berger）表示，植入該設備後，此前經過藥物處理而失去記憶的老鼠重新獲得了記憶能力，“輕輕關閉開關，老鼠會遺忘，打開開關，老鼠會重新想起”；另外，這些老鼠對新信息的記憶能力更強。
該團隊的研究建立在科學家們最近對大腦海馬體及其在學習方面所起作用的理解不斷取得突破的基礎上。在整個學習過程中，海馬體的作用是將短期記憶變成長期記憶。伯格表示：“沒有海馬體，就沒有長期記憶，但仍然會有短期記憶。”
實驗中，小鼠會先後看到兩個外觀一樣的開關，研究者故意分散小鼠的注意力之後，再讓它選擇後出現的那個開關。在多次重複之後，小鼠會記住實驗的規則（選擇後出現的開關），但每次具體選哪一個開關，需要的則是短期記憶（這次開關出現的順序）。
小鼠的腦中被安上了一系列電極，一直連到海馬體的CA1和CA3兩個區。當大腦將信號傳到CA1和CA3時，電極同樣會收到這些信號並進行儲存。然後科學家們用藥物讓小鼠的海馬體CA1區停止了作用，這時，小鼠雖然記得遊戲的規則，卻無法記住自己先看到的是哪一個開關，於是只能亂選一氣。
接著，研究者們將得到信號的電極“打開”，讓它們向海馬體傳遞信號，小鼠立刻重新擁有了短期記憶能力，——換言之，當海馬體CA1區出現了問題時，電極可以起到取而代之的作用。
而在未被藥物影響的小鼠中，記憶力衰退的現像也大大緩解——在較長的“分散注意力”活動之後，未使用電極小鼠的記憶會消散大約40%，而通過電極“強化”相應信號的小鼠們，只損失了10%的記憶。
儘管現在的電極設備只要稍作修改就能裝進人腦，但研究者們表示要投入實用還有許多障礙，比如對於嚴重記憶力受損的患者，腦波信號本身可能很弱、難以通過電極儲存，而且人腦關於記憶的區塊也遠遠多於CA1和CA3，要真的全面提高記憶力，還需要多做研究。接下來，科學家們計劃在靈長類動物身上重複這一實驗，其最終目的是製造出能幫助阿爾茨海默病、中風或傷殘患者的植入物，讓其恢復功能。
這個研究團隊的論文標題為“皮質神經義體恢復和提高記憶力”（A Cortical Neural Prosthesis for Restoring and Enhancing Memory），發表在《神經工程學》（Neural Engineering）期刊上。
http://www.nytimes.com/2011/06/17/science/17memory.html?_r=1
Memory Implant Gives Rats Sharper Recollection
By BENEDICT CAREY
Published: June 17, 2011
Scientists have designed a brain implant that restored lost memory function and strengthened recall of new information in laboratory rats — a crucial first step in the development of so-called neuroprosthetic devices to repair deficits from dementia, stroke and other brain injuries in humans.
Though still a long way from being tested in humans, the implant demonstrates for the first time that a cognitive function can be improved with a device that mimics the firing patterns of neurons. In recent years neuroscientists have developed implants that allow paralyzed people to move prosthetic limbs or a computer cursor, using their thoughts to activate the machines. In the new work, being published Friday, researchers at Wake Forest University and the University of Southern California used some of the same techniques to read neural activity. But they translated those signals internally, to improve brain function rather than to activate outside appendages.
“It’s technically very impressive to pull something like this off, given our current level of technology,” said Daryl Kipke, a professor of bioengineering at the University of Michigan who was not involved in the experiment. “We are just scratching the surface when it comes to interacting with the brain, but this experiment shows what’s possible and the great potential of interacting with the brain in this way.”
In a series of experiments, scientists at Wake Forest led by Sam A. Deadwyler trained rats to remember which of two identical levers to press to receive water; the animals first saw one of the two levers appear and then (after being distracted) had to remember to press the other lever to be rewarded. Repeated training on this task teaches rats the general rule, but in each trial the animal has to remember which lever appeared first, to inform the later choice.
The rats were implanted with a tiny array of electrodes, which threaded from the top of the head down into two neighboring pieces of the hippocampus, a structure that is crucial for forming these new memories, in rats as in humans. The two slivers of tissue, called CA1 and CA3, communicate with each other as the brain learns and stores new information. The device transmits these exchanges to a computer.
To test the effect of the implant, the researchers used a drug to shut down the activity of CA1. Without CA1 online, the rats could not remember which lever to push to get water. They remembered the rule — push the opposite lever of the one that first appeared — but not which they had seen first.
The researchers, having recorded the appropriate signal from CA1, simply replayed it, like a melody on a player piano — and the animals remembered. The implant acted as if it were CA1, at least for this one task.
“Turn the switch on, the animal has the memory; turn it off and they don’t: that’s exactly how it worked,” said Theodore W. Berger, a professor of engineering at U.S.C. and the lead author of the study, being published in The Journal of Neural Engineering. His co-authors were Robert E. Hampson and Anushka Goonawardena, along with Dr. Deadwyler, of Wake Forest, and Dong Song and Vasilis Z. Marmarelis of U.S.C.
In rats that did not receive the drug, new memories faded by about 40 percent after a long distraction period. But if the researchers amplified the corresponding CA1 signals using the implant, the memories eroded only about 10 percent in that time.
The authors said that with wireless technology and computer chips, the system could be easily fitted for human use. But there are a number of technical and theoretical obstacles. For one, the implant must first record a memory trace before playing it back or amplifying it; in patients with significant memory problems, those signals may be too weak. In addition, human memory is a rich, diverse neural process that involves many other brain areas, not just CA3 and CA1; implants in this area will be limited.
Still, some restored memories — Where is the bathroom? Where are the pots and pans stored? — could make a big difference in the lives of someone with dementia. “If you’re caring for someone in the house, for example,” Dr. Berger said, “it might be enough to keep the person out of the nursing home.”
This article has been revised to reflect the following correction:
Correction: June 19, 2011
An article on Friday about a brain implant that improved lost memory function in laboratory rats misidentified the journal in which the research was published. It is The Journal of Neural Engineering , not The Journal of NeuroEngineering and Rehabilitation.
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