Over the years, scientists have come up with a lot of ideas about why we sleep.关于我们为什么要睡，多年来，科学家明确提出了很多点子。Some have argued that it’s a way to save energy. Others have suggested that slumber provides an opportunity to clear away the brain’s cellular waste. Still others have proposed that sleep simply forces animals to lie still, letting them hide from predators.有些人指出这是一种节约能量的方法。其他人明确提出，睡眠中为大脑获取了清理细胞废物的机会。还有一些人指出，睡眠中只是被迫动物静静地躺下来，让它们可以逃过捕食者。
A pair of papers published on Thursday in the journal Science offer evidence for another notion: We sleep to forget some of the things we learn each day.周四在《科学》(Science)期刊上公开发表的两篇论文为另一个观念获取了证据：我们睡是为了记得每天所学到的一些东西。In order to learn, we have to grow connections, or synapses, between the neurons in our brains. These connections enable neurons to send signals to one another quickly and efficiently. We store new memories in these networks.为了自学，我们必需减少大脑神经元之间的相连，或者叫神经元。
这些相连使神经元需要较慢有效地在彼此之间发送到信号。我们就是在这些网络之中存储新的记忆。In 2003, Giulio Tononi and Chiara Cirelli, biologists at the University of Wisconsin-Madison, proposed that synapses grew so exuberantly during the day that our brain circuits got “noisy.” When we sleep, the scientists argued, our brains pare back the connections to lift the signal over the noise.2003年，威斯康星大学麦迪逊分校的生物学家朱利奥·托诺尼(Giulio Tononi)和基娅纳·奇雷利(Chiara Cirelli)明确提出，神经元在白天生长得十分白热化，令其大脑电路显得“喧闹”。
当我们睡觉时,大脑以求增加相连，这样确实的信号才可以多达噪声。In the years since, Dr. Tononi and Dr. Cirelli, along with other researchers, have found a great deal of indirect evidence to support the so-called synaptic homeostasis hypothesis.在此之后的几年里，托诺尼博士和奇雷利博士与其他研究者找到了大量间接证据，反对这一所谓的神经元自稳态假说。
It turns out, for example, that neurons can prune their synapses — at least in a dish. In laboratory experiments on clumps of neurons, scientists can give them a drug that spurs them to grow extra synapses. Afterward, the neurons pare back some of the growth.比如，事实证明，神经元可以遮荫它们的神经元——最少是在实验室里。在对神经元丛展开实验室实验时，科学家给它们一种药物，性刺激它们生长额外的神经元。
之后，神经元缩减了一些生长。Other evidence comes from the electric waves released by the brain. During deep sleep, the waves slow down. Dr. Tononi and Dr. Cirelli have argued that shrinking synapses produce this change.其他证据来自大脑获释的电波。
在深度睡眠中期间，电波减缓。托诺尼博士和奇雷利博士指出，这种变化是由神经元增大带给的。Four years ago, Dr. Tononi and Dr. Cirelli got a chance to test their theory by looking at the synapses themselves. They acquired a kind of deli slicer for brain tissue, which they used to shave ultrathin sheets from a mouse’s brain.四年前，托诺尼博士和奇雷利博士以求通过观察神经元本身来检验他们的理论。他们取得了一种用作脑组织的切片机，用它从小鼠的大脑上获得超薄切片。
Luisa de Vivo, an assistant scientist working in their lab, led a painstaking survey of tissue taken from mice, some awake and others asleep. She and her colleagues determined the size and shape of 6,920 synapses in total.该实验室的助理科学家路易莎·德·维沃(Luisa de Vivo)对这些从小鼠大脑放入的的组织展开了精心研究，一些小鼠是醒着的，其他一些正处于睡眠中状态。她和同事们确认了6920个神经元的大小和形状。
The synapses in the brains of sleeping mice, they found, were 18 percent smaller than in awake ones. “That there’s such a big change over all is surprising,” Dr. Tononi said.他们找到，睡眠中小鼠脑中的神经元比精神状态小鼠的神经元小18％。“整体而言，那个极大的变化极为难以置信，”托诺尼博士说道。The second study was led by Graham H. Diering, a postdoctoral researcher at Johns Hopkins University. Dr. Diering and his colleagues set out to explore the synaptic homeostasis hypothesis by studying the proteins in mouse brains. “I’m really coming at it from this nuts-and-bolts place,” Dr. Diering said.第二项研究由约翰霍普金斯大学博士后研究员格雷厄姆·H·迪林(Graham H. Diering)领导。
迪林博士和同事们通过研究小鼠脑中的蛋白质来探寻神经元自稳态假说。“我知道就是指这种细节抵达来研究这个问题的，”迪林博士说道。In one experiment, Dr. Diering and his colleagues created a tiny window through which they could peer into mouse brains. Then he and his colleagues added a chemical that lit up a surface protein on brain synapses.在一个实验中，迪林博士和同事们创立了一个小窗口，通过它可以窥看小鼠的大脑。
然后，他和同事们在小鼠大脑内加到了一种化学物质，需要照亮脑神经元上的表面蛋白。Looking through the window, they found that the number of surface proteins dropped during sleep. That decline is what you would expect if the synapses were shrinking.利用窗口，他们找到，在睡眠中期间神经元表面蛋白的数量上升。
如果神经元增大，这种上升就应当不会经常出现。Dr. Diering and his colleagues then searched for the molecular trigger for this change. They found that hundreds of proteins increase or decrease inside of synapses during the night. But one protein in particular, called Homer1A, stood out.迪林博士和同事们随后开始找寻这种变化的分子启动时因素。他们找到，在神经元内，有数百种蛋白质在夜间减少或增加。但有一种取名为Homer1A的蛋白质十分引人注目。
In earlier experiments on neurons in a dish, Homer1A proved to be important for paring back synapses. Dr. Diering wondered if it was important in sleep, too.在对神经元展开的早期实验室实验中，Homer1A被证明在神经元增加过程中充分发挥了最重要起到。迪林博士想要告诉它否在睡眠中也很最重要。To find out, he and his colleagues studied mice genetically engineered so that they couldn’t make Homer1A proteins. These mice slept like ordinary mice, but their synapses didn’t change their proteins like the ones in ordinary mice.为了找到这一点，他和同事研究了经基因工程改建、无法生产Homer1A蛋白的小鼠。
这些小鼠可以像普通小鼠一样睡，但是它们的神经元不像在普通小鼠中那样转变其蛋白质。Dr. Diering’s research suggests that sleepiness triggers neurons to make Homer1A and ship it into their synapses. When sleep arrives, Homer1A turns on the pruning machinery.迪林博士的研究指出，困倦引起神经元生产Homer1A，并将其载运到神经元。当睡眠中开始时，Homer1A也关上了它的遮荫机制。To see how this pruning machinery affects learning, the scientists gave regular mice a memory test. They put the animals in a room where they got a mild electric shock if they walked over one section of the floor.为了仔细观察这种遮荫机制如何影响自学，科学家对普通小鼠展开了记忆测试。
他们把这些动物放到一个房间里，如果它们回头到地板的某一部分，就不会受到严重的电击。That night, the scientists injected a chemical into the brains of some of the mice. The chemical had been shown to block neurons in dishes from pruning their synapses.当天晚上，科学家将一种化学物质流经若干小鼠的脑中。在实验室中，这种化学物质已被证明可以制止神经元增加其神经元。
The next day, the scientists put all the mice back in the chamber they had been in before. Both groups of mice spent much of the time frozen, fearfully recalling the shock.第二天，科学家把所有小鼠都取出之前所在的房间。两组小鼠大部分时间都是一动不动，不安地回忆起电击的记忆。But when the researchers put the mice in a different chamber, they saw a big difference. The ordinary mice sniffed around curiously. The mice that had been prevented from pruning their brain synapses during sleep, on the other hand, froze once again.但当研究人员把老鼠放进有所不同的房间，他们看见了相当大的区别。
普通组的老鼠奇怪地四处腺着。另一边，在睡眠中期间被制止增加大脑神经元的小鼠再度一动不动。Dr. Diering thinks that the injected mice couldn’t narrow their memories down to the particular chamber where they had gotten the shock. Without nighttime pruning, their memories ended up fuzzy.迪林博士指出，不受静脉注射的小鼠无法把记忆增大到它们遭到电击的特定房间范围内。没夜间的遮荫，它们的记忆最后显得模糊不清。
In their own experiment, Dr. Tononi and his colleagues found that the pruning didn’t strike every neuron. A fifth of the synapses were unchanged. It’s possible that these synapses encode well-established memories that shouldn’t be tampered with.在他们自己的实验中，托诺尼博士和同事们找到，遮荫并不是针对每个神经元。1/5的神经元没转变。有可能这些神经元之中编码了早已较好地创建一起、且不该被改动的记忆。“You can forget in a smart way,” Dr. Tononi said.“你可以用一种聪慧的方式来记得，”托诺尼博士说道。
Other researchers cautioned that the new findings weren’t definitive proof of the synaptic homeostasis hypothesis.其他研究者警告说道，新的找到并无法为神经元自稳态假说获取决定性的证据。Marcos G. Frank, a sleep researcher at Washington State University in Spokane, said that it could be hard to tell whether changes to the brain at night were caused by sleep or by the biological clock. “It’s a general problem in the field,” he said.华盛顿州立大学斯波坎分校的睡眠中问题研究者马科斯·G·弗兰克(Marcos G. Frank)说道，很难辨别大脑夜间的变化是由睡眠中还是生物钟引发的。“这是该领域的一个广泛问题，”他说道。
Markus H. Schmidt, of the Ohio Sleep Medicine Institute, said that while the brain might prune synapses during sleep, he questioned whether this was the main explanation for why sleep exists.俄亥俄睡眠中医学研究所(Ohio Sleep Medicine Institute)的马库斯·H·施密特(Markus H. Schmidt)说道，虽然大脑有可能在睡眠中期间遮荫神经元，但他批评这一点是否是睡眠中不存在的主要原因。“The work is great,” he said of the new studies, “but the question is, is this a function of sleep or is it the function?”“这项工作很好，”他谈到这项新的研究时说，“但问题是，这是睡眠中的功能之一，还是它的主要功能？”Many organs, not just the brain, seem to function differently during sleep, Dr. Schmidt pointed out. The gut appears to make many new cells, for example.不仅大脑，许多器官在睡眠中时的功能或许都不一样，施密特博士认为。比如肠道或许就不会产生许多新的细胞。Dr. Tononi said that the new findings should prompt a look at what current sleeping drugs do in the brain. While they may be good at making people sleepy, it’s also possible that they may interfere with the pruning required for forming memories.托诺尼博士说道，新的找到可以促成人们检视目前的睡眠中药物在大脑中充分发挥什么起到。
虽然它们可以让人们深感困意，但它们也有可能阻碍构成记忆所需的神经元遮荫。“You may actually work against yourself,” Dr. Tononi said.“你有可能只不过是在伤害自己，”托诺尼博士说道。
In the future, sleep medicines might precisely target the molecules involved in sleep, ensuring that synapses get properly pruned.在将来，睡眠中药物也许可以准确射击参予睡眠中的分子，保证神经元获得必要的遮荫。“Once you know a little bit of what happens at the ground-truth level, you can get a better idea of what to do for therapy,” Dr. Tononi said.“一旦你告诉一点基本事实层面再次发生的情况，就可以获得更佳的化疗思路，”托诺尼博士说道。
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