人爲什麼需要睡眠?爲了遺忘大綱

Over the years, scientists have come up with a lot of ideas about why we sleep.
關於我們爲什麼要睡覺，多年來，科學家提出了很多想法。

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.
有些人認爲這是一種節約能量的方法。其他人提出，睡眠爲大腦提供了清除細胞廢物的機會。還有一些人認爲，睡眠只是迫使動物靜靜地躺下來，讓它們可以躲過捕食者。

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.
週四在《科學》(Science)期刊上發表的兩篇論文爲另一個觀念提供了證據：我們睡覺是爲了忘記每天所學到的一些東西。

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.
爲了學習，我們必須增加大腦神經元之間的連接，或者叫突觸。這些連接使神經元能夠快速有效地在彼此之間發送信號。我們就是在這些網絡之中存儲新的記憶。

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，威斯康星大學麥迪遜分校的生物學家朱利奧·託諾尼(Giulio Tononi)和基婭拉·奇雷利(Chiara Cirelli)提出，突觸在白天生長得非常激烈，令大腦電路變得“嘈雜”。當我們睡覺時,大腦得以減少連接，這樣真正的信號纔可以超過噪聲。

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.
在此之後的幾年裏，託諾尼博士和奇雷利博士與其他研究者發現了大量間接證據，支持這一所謂的突觸自穩態假說。

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，事實證明，神經元可以修剪它們的突觸——至少是在實驗室裏。在對神經元叢進行實驗室實驗時，科學家給它們一種藥物，刺激它們生長額外的突觸。之後，神經元削減了一些生長。

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.
其他證據來自大腦釋放的電波。在深度睡眠期間，電波減慢。 託諾尼博士和奇雷利博士認爲，這種變化是由突觸縮小帶來的。

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，託諾尼博士和奇雷利博士得以通過觀察突觸本身來檢驗他們的理論。他們獲得了一種用於腦組織的切片機，用它從小鼠的大腦上得到超薄切片。

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.
該實驗室的助理科學家路易莎·德·維沃(Luisa de Vivo)對這些從小鼠大腦取出的組織進行了精心研究，一些小鼠是醒着的，其他一些處於睡眠狀態。她和同事們確定了6920個突觸的大小和形狀。

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.
他們發現，睡眠小鼠腦中的突觸比清醒小鼠的突觸小18％。“整體而言，那個巨大的變化頗爲驚人，”託諾尼博士說。

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.
第二項研究由約翰霍普金斯大學博士後研究員格雷厄姆·H·迪林(Graham H. Diering)領導。迪林博士和同事們通過研究小鼠腦中的蛋白質來探索突觸自穩態假說。“我真的是從這種細節出發來研究這個問題的，”迪林博士說。

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.
在一個實驗中，迪林博士和同事們創建了一個小窗口，通過它可以窺看小鼠的大腦。然後，他和同事們在小鼠大腦內添加了一種化學物質，能夠點亮腦突觸上的表面蛋白。

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.
透過窗口，他們發現，在睡眠期間突觸表面蛋白的數量下降。如果突觸縮小，這種下降就應該會出現。

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.
迪林博士和同事們隨後開始尋找這種變化的分子觸發因素。他們發現，在突觸內，有數百種蛋白質在夜間增加或減少。但有一種名爲Homer1A的蛋白質格外突出。

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.
在對神經元進行的早期實驗室實驗中，Homer1A被證明在突觸減少過程中發揮了重要作用。迪林博士想知道它是否在睡眠中也很重要。

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.
爲了發現這一點，他和同事研究了經基因工程改造、不能製造Homer1A蛋白的小鼠。這些小鼠可以像普通小鼠一樣睡覺，但是它們的突觸不像在普通小鼠中那樣改變其蛋白質。

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.
迪林博士的研究表明，睏倦引發神經元製造Homer1A，並將其運送到突觸。當睡眠開始時，Homer1A也打開了它的修剪機制。

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.
爲了觀察這種修剪機制如何影響學習，科學家對普通小鼠進行了記憶測試。他們把這些動物放在一個房間裏，如果它們走到地板的某一部分，就會受到輕微的電擊。

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.
當天晚上，科學家將一種化學物質注入若干小鼠的腦中。在實驗室中，這種化學物質已被證明可以阻止神經元減少其突觸。

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，科學家把所有小鼠都放回之前所在的房間。兩組小鼠大部分時間都是一動不動，恐懼地回憶起電擊的記憶。

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.
但當研究人員把老鼠放入不同的房間，他們看到了很大的區別。普通組的老鼠好奇地到處嗅着。另一邊，在睡眠期間被阻止減少大腦突觸的小鼠再次一動不動。

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.
迪林博士認爲，受注射的小鼠不能把記憶縮小到它們遭受電擊的特定房間範圍內。沒有夜間的修剪，它們的記憶最後變得模糊。

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.
在他們自己的實驗中，託諾尼博士和同事們發現，修剪並不是針對每個神經元。1/5的突觸沒有改變。有可能這些突觸之中編碼了已經良好地建立起來、且不應被修改的記憶。

“You can forget in a smart way,” Dr. Tononi said.
“你可以用一種聰明的方式來忘記，”託諾尼博士說。

Other researchers cautioned that the new findings weren’t definitive proof of the synaptic homeostasis hypothesis.
其他研究者警告說，新的發現並不能爲突觸自穩態假說提供決定性的證據。

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.
華盛頓州立大學斯波坎分校的睡眠問題研究者馬科斯·G·弗蘭克(Marcos G. Frank)說，很難判斷大腦夜間的變化是由睡眠還是生物鐘引起的。“這是該領域的一個普遍問題，”他說。

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.
俄亥俄睡眠醫學研究所(Ohio Sleep Medicine Institute)的馬庫斯·H·施密特(Markus H. Schmidt)說，雖然大腦可能在睡眠期間修剪突觸，但他質疑這一點是否是睡眠存在的主要原因。

“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?”
“這項工作很好，”他談起這項新研究時說，“但問題是，這是睡眠的功能之一，還是它的主要功能？”

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.
不僅大腦，許多器官在睡眠時的功能似乎都不一樣，施密特博士指出。比如腸道似乎就會產生許多新的細胞。

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.
託諾尼博士說，新的發現可以促使人們審視目前的睡眠藥物在大腦中發揮什麼作用。雖然它們可以讓人們感到睏意，但它們也可能干擾形成記憶所需的突觸修剪。

“You may actually work against yourself,” Dr. Tononi said.
“你可能其實是在損害自己，”託諾尼博士說。

In the future, sleep medicines might precisely target the molecules involved in sleep, ensuring that synapses get properly pruned.
在將來，睡眠藥物或許可以精確瞄準參與睡眠的分子，確保突觸得到適當的修剪。

“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.
“一旦你知道一點基本事實層面發生的情況，就可以得到更好的治療思路，”託諾尼博士說。