If such a snooze button exists in humans, it could protect against strokes, heart attacks and trauma
於人類中，倘若存在這種打盹按鈕，則可能防止中風、心臟病發作及創傷。
圖1. 於洞穴中冬眠的榛樹睡鼠(Muscardinus avellanarius) (圖援用自原文)
A well-worn science-fiction trope imagines space travelers going into suspended animation as they head into deep space. Closer to reality are actual efforts to slow biological processes to a fraction of their normal rate by replacing blood with ice-cold saline to prevent cell death in severe trauma. But saline transfusions or other exotic measures are not ideal for ratcheting down a body’s metabolism because they risk damaging tissue.
一部陳舊的科幻小說，幻想太空旅人前往深太空(太陽系以外的宇宙太空)時，進入生命功能暫時停止狀態。較接近現實的是，實際嘗試藉由使用冰冷生理鹽水代替血液，來防止嚴重創傷中的細胞死亡，以使生物過程減緩到正常速率的一小部分。但是生理鹽水注入或其他外來的方法，對於降低人體新陳代謝，不是理想的選擇。因為，它們冒用損傷組織的風險。
Coaxing an animal into low-power mode on its own is a better solution. For some animals, natural states of lowered body temperature are commonplace. Hibernation is the obvious example.
誘使動物自身進入低功率模式，是一種較佳的解決方法。就某些動物而言，常有降低體溫的自然情況，冬眠是最明顯的例子。
When bears, bats or other animals hibernate, they experience multiple bouts of a low-metabolism state called torpor for days at a time, punctuated by occasional periods of higher arousal. Mice enter a state known as daily torpor, lasting only hours, to conserve energy when food is scarce.
當熊、蝙蝠或其他動物冬眠時，牠們一次連續多日、經歷多次，被稱為休眠的低代謝狀態，偶爾遭較高度甦醒的時間打斷。當食物匱乏時，為了保持能量，小鼠進入維持僅數小時，被通稱為每日休眠的狀態。
The mechanisms that control torpor and other hypothermic states—in which body temperatures drop below 37 degrees Celsius—are largely unknown. Two independent studies published in Nature on Thursday identify neurons that induce such states in mice when they are stimulated.
控制休眠狀態及其他低溫狀態(體溫下降低於37℃)的機制，大半不詳。兩項發表於2020年6月11日(星期四)《自然》期刊的獨立研究確認了，在遭受刺激時的小鼠中，誘發這種狀態的神經元。
The work paves the way toward understanding how these conditions are initiated and controlled. It could also ultimately help find methods for inducing hypothermic states in humans that will prove useful in medical settings. And more speculatively, such methods might one day approximate the musings about suspended animation that turn up in the movies.
這種研究為邁向瞭解此些狀況，如何被啟動及控制鋪了路。這最終也可能有助於，在人類中找到誘發，於醫療背景中，能證明是有用之低體溫狀態的方法。更思索性的是，有朝一日，這類方法可能近似，於電影中，出現之有關生命功能，暫時停止狀態的冥想。
One of the two studies was conducted by neuroscientist Takeshi Sakurai of the University of Tsukuba in Japan and his colleagues. It began with a paradoxical finding about a peptide called QRFP. The team showed that injecting it into animals actually increased their activity. But when the researchers switched on neurons that were making the peptide in mice, they got a surprise.
這兩項研究之一，是由日本筑波大學神經科學家，Takeshi Sakurai及其同僚們進行。這以一項有關，被稱為QRFP之肽的發現開始。該團隊證實，將其注入動物體內，實際上增強了牠們的活動力。不過，當此些研究人員開啟，於小鼠中，導致這種肽的神經元時，他們感到很訝異。
“The mice stayed still and were very cold: the opposite to what they expected,” says Genshiro Sunagawa, of the RIKEN Center for Biosystems Dynamics Research in Japan, who co-led the study. The animals’ metabolic rate (measured by oxygen consumption), body temperature, heart rate and respiration all dropped.
該項研究共同領導人，日本物理暨化學研究所(RIKEN：Rikagaku Kenkyusho)生物系統動力學研究中心的Genshiro Sunagawa宣稱：「此些小鼠靜止不動且非常冷，這與他們預期的相反。」此些動物的代謝率(以耗氧量衡量)、體溫、心率及呼吸全下降。
QRFP itself was not involved in altering the mice’s metabolic rate. In fact, the lowered body temperature and other measures did not disappear when the gene for the peptide was deleted. But the gene appeared to serve as a landmark that could steer researchers to relevant metabolism-lowering neurons.
QRFP本身不涉及改變小鼠的代謝率。實際上，當刪除代表該種肽的基因時，下降的體溫及其他計量並未消失。不過，該基因顯然充當一種，可能引領研究人員們找尋，降低新陳代謝有關聯之神經元的地標。
The QRFP peptide is found in many parts of the body, but it is especially prevalent in the hypothalamus, a brain region important for thermoregulation. Knowing this, the researchers used a technique known as chemogenetics—in which neurons are genetically modified so that they can be activated using a drug—to look for neurons in the hypothalamus responsible for the effect.
QRFP這種肽，於身體諸多部位中被發現。不過，在下丘腦(對溫度調節很重要的大腦區域)中，特別普遍。知曉這一點，此些研究人員使用了一種，被通稱為化學遺傳學的技術(在此神經元經遺傳修飾，以便能使用藥物激活)，來找尋下丘腦中，導致此作用的神經元。
They found that activating QRFP neurons indiscriminately produced a state that lasted for hours. And selectively activating neurons in specific parts of the hypothalamus sent the animals into a hibernationlike condition that lasted more than two days.
他們發現，激活QRFP的神經元，無差別地產生了，持續幾個小時的狀態。而選擇性激活下丘腦特定部位中的神經元，使此些動物進入一種，持續了兩天以上的冬眠樣狀態。
During this period, the mice’s metabolism remained properly regulated. And afterward, the rodents revived spontaneously—and unharmed, just as with hibernation. The team called these particular cells Q neurons and named the state the animals were in Q-neuron-induced hypothermia and hypometabolism (QIH). More simply, these properties describe torpor or hibernation.
在此期間，這些小鼠的新陳代謝保持適當調節。因此，就如同冬眠，沒受到傷害。該團隊稱這些特殊細胞為Q神經元，並指出這些動物是處於，Q神經元誘發之低體溫及低新陳代謝(QIH)的狀態。更簡單地說，這些特性說明了，休眠或冬眠的狀態。
The researchers conducted a similar experiment in rats, which do not naturally enter torpor, and saw the same effect. Even mice do not naturally hibernate for days at a time, as they did in these experiments. It is possible the animals’ reduced metabolism extended the effects of the drug, which normally wears off in around four hours.
在沒有自然進入休眠狀態的大鼠中，此些研究人員進行了類似實驗，且看到了相同效果。即使是小鼠，也沒有如同牠們在這些實驗中，自然冬眠一次達數天。這可能是此些動物降低的新陳代謝，擴展了該種藥物，通常會在四個小時內消失的作用。
But Sunagawa favors another explanation: “Maybe it’s like pressing a switch. And after that, some other systems maintain the condition for a while,” he says. “We believe this system might exist in other mammals.”
不過，Sunagawa贊成另一種解釋。他宣稱：「也許這如同按一個開關。在那之後，其他一些系統維持這種狀況一段時間。他們認為，該種系統可能存在於，其他哺乳動物中。」
The second study, led by neurobiologist Sinisa Hrvatin of Harvard Medical School, induced torpor in mice by depriving them of food. The team used chemogenetic tools to modify neurons that were active as the animals entered torpor, causing them to produce a receptor that could be turned on by a drug.
由美國哈佛醫學院神經生物學家，Sinisa Hrvatin領導的第二項研究，於小鼠中，藉由剝奪其食物，誘發了休眠狀態。該團隊使用了，化學遺傳工具來修飾，當動物進入休眠狀態時，是活躍的神經元。這導致牠們產生一種，能被藥物開啟的受體。
It later injected these mice with the drug to reactivate the neurons and found that doing so induced a torporlike state even when food was available, which lowered the animals’ metabolism.
後來，以該種藥物注射此些小鼠，來重新激活此些神經元。結果發現，這麼做即使在有食物的情況下，也誘發了降低此些動物新陳代謝之類似休眠的狀態。
“The question was: If we captured brain activity in torpor, then later restimulated those neurons, is that sufficient to induce torpor?” Hrvatin says. “We were amazed that the answer was yes.”
Hrvatin宣稱：「問題是：倘若我們捕獲了，於休眠狀態中的大腦活動。那麼隨後重新刺激了那些神經元，是否足以誘發休眠狀態？他們很驚訝，答案是肯定的。」
The researchers showed that activating neurons in the same area in the hypothalamus where Sakurai and his colleagues found Q neurons was enough to initiate torpor. They also blocked the activity of these neurons, which disrupted the mice’s ability to enter torpor.
此些研究人員證實，激活於Sakurai及其同僚們發現Q神經元之相同區域的神經元，足以引發休眠狀態。他們也阻擾了，這些神經元的活動。這擾亂了，小鼠進入休眠狀態的能力。
“When you do a study like this, you’re out on a limb,” says neuroscientist Michael Greenberg, who was senior author of the second paper. “So when two studies come from such different perspectives and seem to unify something, it’s gratifying and a relief.”
第二項論文的資深撰文人，神經科學家Michael Greenberg宣稱：「當進行類似上述研究時，是處於孤立的。因此，當兩項研究，來自如此不同層面，且似乎統一了某事物時，這是令人滿意且欣慰的。」
The research provides new insight into a brain region known for its role in controlling basic bodily states.
該項研究提供了，大腦在控制基本身體諸狀態中，因其角色聞名之區域的新洞察力。
“We knew that the hypothalamus coordinates the majority of the body’s autonomic processes, like thermoregulation, circulation, body weight and energy balance,” says physiologist Gerhard Heldmaier of Philipps University of Marburg in Germany, who was not involved in the work. “From these studies, we learn that hypothalamic neurons guarantee not only stability but can also shift this control from life in the fast lane to life in the slow lane.”
德國馬爾堡菲利普斯大學，未涉及該項研究的生理學家，Gerhard Heldmaier宣稱：「我們知曉，下丘腦協調諸如體溫調節、血液循環、體重及能量平衡等，大多數人體自主神經的變化過程。從這些研究，我們得悉，下丘腦的神經元不僅保證穩定性，也能將這種控制，從快車道中的生命現象轉移到慢車道中的生命現象。」
A key next step will be to study more species. “It will be interesting to see how these cells differ between hibernators and nonhibernators,” Heldmaier says. “And if proper activation of them induces hibernation in nonhibernators.”
關鍵的下一步，將是研究更多物種。Heldmaier宣稱：「瞭解此些細胞，在冬眠者與非冬眠者之間的差異，會是令人感興趣的。如果適當激活它們，則在非冬者中，能誘發冬眠。」
A focus will be understanding how this biological system works. “What does it mean for a cell to be in torpor?” Hrvatin asks. “If you understand this at a molecular level, you may be able to protect the brain from ischemic injury, such as the most common type of stroke, or even neurodegenerative diseases.” Similar considerations apply to preserving organs for transplant.
關注的焦點將是瞭解，此生物系統如何運作。Hrvatin質疑：「細胞處於休眠狀態，意味著什麼？倘若以分子層級瞭解這一點，或許能保護大腦免於，諸如最常見之中風類型的缺血性損傷，或甚至神經退行性疾病。」類似的考慮也適用於，保存供移植的器官。
Whether these states could be induced in humans remains to be seen. Small mammals have very different temperature-regulation systems than those of large mammals, so it is not clear if these neurons will have the same effect. “Is it possible to change the set point in a human? And by how much? I don’t know,” Hrvatin says.
這些狀態能否在人類中被誘發，仍有待瞭解。小型哺乳動物具有極不同於，那些大型哺乳動物的溫度調節系統。因此，不清楚這些神經元是否會具有相同作用。Hrvatin宣稱：「於人類中，可能改變此決定點？可達多少？我不知道。」
“There are a lot of unanswered questions.” Sunagawa dreams of intervals of “daily hibernation.” “If we could understand what sleep is doing, maybe we could combine sleeping and hibernation” and slow aging down, he says. Sunagawa’s group’s paper in Nature even includes a passage that speculates about inducing this quiescent state for astronauts going into deep space.
Sunagawa夢想著間歇性的“每日休眠”，這“有很多未解決的問題”。他宣稱：「倘若能瞭解睡眠在做什麼，或許能結合睡眠及冬眠，來延緩老化。」
Sunagawa團隊於《自然》期刊中的論文甚至包括了，一段思索有關為進入深太空之宇航員，誘發這種休止狀態的章節。
原文網址：https://www.scientificamerican.com/article/switch-in-mouse-brain-induces-a-deep-slumber-similar-to-hibernation/
翻譯：許東榮
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