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Text 1

Are Dreams as Vital as Sleep?

by Roger Louis

 

    Can dreams be controlled at our own will? Is dreaming the ability of all animals? How do the deaf-mutes and the mentally disabled dream? The following article discusses these issues. 

    Sooner or later biologists were bound to investigate one of the brain's most mysterious functions, probably the least tangible and the least comprehensible function of the body, dreaming. 

    Just a few years ago we thought that Freud, when he took the keys to the city of dreams away from the philosophers and poets, had given them once and for all to the psychologists and psychiatrists. But now biologists, biochemists and neuropsychologists are invading what used to be thought an exclusive preserve. 

    One of these is a Frenchman, Dr. Michel Jouvet, whose research at the medical school of Lyons is internationally recognized as authoritative and on the same plane as that of Professor Nathaniel Kleitman in the United States, which has been continued since 1960 by one of his colleagues, Dr. William Dement.

    It was more or less by chance that Dr. Jouvet became interested in dreams in 1958, or rather it was the logic inherent in any experimental work that stimulated his curiosity. 

    "I was interested at that time in confirming Pavlov's theories of conditioning, using cats as test animals," he told us. "We had put electrodes in the muscles of their paws in order to check on certain movements." 

    "During their sleep we noted an unexpected phenomenon that occurred sporadically—the complete disappearance of muscular tone, sometimes lasting for several minutes, after which muscular tone reappeared while the animal continued to sleep. 

    "We thought of all possible theories to explain this phenomenon. It even occurred to us that it might be connected with the very special role that whiskers play in the cat, and we actually tried cutting them off to see whether this might have some effect. Only after a long period of groping, did we realize that there was a possible correlation with dreaming." 

    "From that moment our research was directed towards the physiological study of sleep, especially towards what we now call its paradoxical phase. This corresponds to the period in which an animal or a person dreams." 

    "This research was carried out in collaboration with Kleitman and Dement in the United States, among others. In a very short time we were able to collect an extraordinary amount of information and numerous records." 

    "We might begin with the most basic points. By mere physical examination of a person or an animal who is sound asleep, we can now tell whether he is dreaming or not; better yet, we can identify, to within one second, the instant he begins to dream and the instant his dream ends." 

    "We have three basic physiological criteria for this finding, and they are now accepted by all neurophysiologists: 

    1. Virtually complete disappearance of muscle tone. 

    2. Rapid eye movements (hence the term REM sleep), which seem to be without purpose. 

    3. Characteristic brain waves on the electroencephalogram, quite different from those recorded in deep sleep and very similar to those recorded in the waking state. Discovery of this tracing gave rise to the term "paradoxical phase," which we apply to sleep in the dreaming state. 

    "We can also state that the average adult dreams about twenty per cent of the time he is asleep, in a number of separate dreams. Each dream episode, about twenty minutes, is preceded by a period of deep sleep, indicated on the encephalographic record by typical long waves. 

    "While we are talking statistics, we might add that the newborn infant dreams much more than the adult—fifty percent of his sleeping time—and this applies to all mammals. 

    "I might also point out that the capability for dreaming is not an attribute of all animal species. In the evolutionary scale it first appears with birds and with them only to a limited degree—about point five percent of their sleeping time. All studies in reptiles and amphibians (e.g. tortoises) give negative results—there are no dreams in their sleep. 

    "This gives a brief summary of recent findings, which will enable us to make a detailed study of the problems still confronting neurophysiologists in the phenomena of dreams as well as in the essential function of dreaming. We are now convinced that dreams play an important physiological role, although we are not yet in a position to say just what that role is. 

    One solitary cat was crouched on a brick in the middle of a miniature pool and sleeping peacefully while an electroencephalograph recorded his brain waves. "We keep him from dreaming," Dr. Jouvet said, "I just explained that one of the recognized physiological criteria of the dream phase in animals is disappearance of muscular tone. This cat can sleep on his brick, but as soon as he begins to dream his muscular tone disappears, and he falls into the water. This at once wakes him up, he climbs back on his brick, licks himself and goes back to sleep—but whenever he dreams he falls into the water again. 

    "If we continue the experiment for a week and then put him back in his cage, we observe that he has such a need to dream that, instead of spending only twenty percent of his sleep time dreaming, he will then spend forty percent of it or more. A kind of compensatory mechanism exists somewhere in his nervous system. 

    "For this reason we think that dreaming is not a pointless phenomenon that occurs every time the nervous system goes into free wheeling, but that it reflects a specific activity of the brain and forms an essential part of a process. As to what the process is, that is what we are trying to discover. 

    "In recent times we have made great progress in localizing the centers responsible for the phenomena that accompany dreaming activity. At first we had to proceed by surgical guesswork, successively removing various parts of the brain stem of our experimental animals in order to observe any disturbance in their sleeping behavior. 

    "Sleep itself is a highly complex phenomenon, and it had not yet been decided whether there is a brain center responsible for sleep or whether simple inhibition of the waking centers is what causes it. 

    "However, we have succeeded in precisely pinpointing the centers responsible for the two principal characteristics of dreaming activity: first, rapid eye movement, which we call phase phenomenon and second, the blocking of muscular tone, which is called a tonic phenomenon.

 

    Cats in a state of hallucination

    "Taken together, these two centers are about the size of a pea. They are located very close to one another, but we can influence either one at will by different techniques. The center controlling muscular tone, which is no bigger than a grape seed, lives his dreams. The powerful blockade of muscular tone is no longer effective, so that the sleeping and dreaming animal carries out all the movements that correspond to the action of his dream. An innocent bystander would get the impression that he was wide awake and perhaps dangerous, but in actual fact none of his actions or gestures corresponds to the outside world in which he is moving. He is asleep and he acts only in accordance with the fantasies that are passing through his brain. He is living in an imaginary world—he is hallucinating. 

    "As soon as he wakes up, his behavior will become quite normal.

"In this experiment you can appreciate the importance of this center: its role in dreaming is primordial. Work is now in progress to study a possible correlation between these hallucinatory states and certain mental illnesses. 

    You might think that sleepwalking would be due to improper functioning of this center, but recent experiments have shown that this phenomenon occurs not during dream periods but in the half awake. People may also talk at this level of sleep—not during dreams. 

    "Another related question is whether the weightlessness experienced in cosmic flights may not have unexpected and undesirable effects upon the astronauts insofar as it creates a state equivalent to the absence of muscular tone. It is not a coincidence that the physician chosen to participate in the first trip to the moon planned by the Americans is a specialist in sleep.

 

    Dreaming can be regulated at will

"But study of the biochemistry of the phenomenon associated with dreams will probably lead to the most fascinating results, and gives us scope to formulate the boldest hypotheses. In the past few years, chemistry has occupied a solid position in the study of biologic phenomena. 

    "Neurohumoral processes of the brain are immensely intriguing to present-day research men, who expect to find in them the key to the most complex phenomena. 

    "Hyden's studies, to cite one example, convincingly show that biochemistry can open a new point of view on biologic phenomena as complicated as memory. This is also true of our studies on dreaming. The REMs, which appear to be at the origin of the dream stage of sleep, can be blocked or amplified by chemical inhibitors or precursors. In other words, it is possible, by means of specific drugs, to deprive an animal of dreams entirely or to increase them to sixty percent of the time he sleeps. 

    "I can offer only one hypothesis, which is directing our study. It is difficult to verify in the present state of our knowledge, but so far nothing contradicts it. Here it is: dreaming activity is inseparable from other activities of the nervous system. There are not separate states of waking, sleeping, dreaming; these phenomena make up a continuum that is characteristic of certain creatures. In the waking state our nervous system, particularly the brain, perceives a certain number of sensations and records or memorizes them in chemical form by synthesizing molecules of specific proteins. This synthesis takes place through a highly complex process. 

    "This conversion of incoming information into a coded chemical schema is not instantaneous. The chemical factory of our brain needs time to store, select and classify information according to a code that is still to be defined. We might say that the waking state is equivalent to recording information on a dictaphone; during deep sleep this information is typed out; and in the course of dreaming, each page or each sentence, or even each word is classified in a file cabinet along with previous information that is stored away in terms of a careful, previously-established code. 

    "This would explain why our dreams contain numerous images corresponding to impressions received in the waking state, and also why some of this information is completely deformed or symbolized. This synthesis of events of the day in dreams would imply a "trituration" of information, together with a review of previous information already classified and coded. 

    "This hypothesis would also explain why newborn infants and young animals have a high percentage of dreaming time—more than twice as much as adults. 

    "I must admit that this hypothesis, although it links dreams to learning and memory, encounters a number of obstacles, it fails to explain why this function suddenly appears in the evolution of species with the bird, to be magnified in a kind of explosion with the mammals. 

    "We must wait some years for the neurophysiologists to carry out further experiments and to interpret them; but it seems to be already well-established that dreams have once and for all left the world of unreality for the world of the laboratory."

(1894 words) TOP


 

课文一

梦与睡眠一样重要吗?

罗杰·露易丝


   我们是否能根据自己的意愿来控制梦境?所有动物都能做梦吗?聋哑人和弱智者怎样做梦?下面这篇文章将讨论这些问题。


    生物学家们迟早会去探究梦这个大脑最神秘的一个功能,可能是最难以触摸、难以理解的人体功能。


    只是在几年以前,我们以为弗洛依德从哲学家和诗人那儿拿走打开梦境之城的钥匙,并将它们永远地留给心理学家与精神分析学家。但现在生物学家,生物化学家以及神经心理学家正在侵入这片曾经被认为是神圣不可侵犯的领地。



   他们其中的一位是法国人米歇尔·儒弗博士,他在里昂医学院的研究被国际公认为同美国纳桑尼尔·克莱特曼教授的研究一样具有权威性,处于同一个层面。克莱特曼的研究自1960年以来由他的同事威廉·第门特继续下来。

   儒弗博士1958年对梦的研究产生兴趣,这或多或少是碰巧的事情,或者说,是实验性工作内含的逻辑性引发了他的好奇。



    “我当时对证明巴甫洛夫的条件理论感兴趣,用猫作为实验动物,”他告诉我们。“我们将电极植入猫爪的肌肉中,来检验某些运动,。”



    “在它们的睡眠中,我们注意到了一种断续发生的出人意料的现象
——肌肉紧张的完全消失,有时延续几分钟,之后肌肉紧张重新出现,而动物继续睡觉。



    “我们想到了用各种可能的理论来解释这一现象。我们甚至觉得猫须的特殊作用可能与这一现象有联系,而且我们实际上试着将猫须剪掉,看这是否起些作用。经过长期的摸索后,我们才意识到这可能与做梦有关。”



    “从那时起,我们的研究转向了对睡眠的生理研究,特别是转向了我们所指的反常阶段。这一阶段与动物或人做梦的时期是一致的。”



    “这一研究是与美国的克莱特曼和第门特等合作进行的。不久,我们就收集了大量的信息与丰富的记录。”



    “我们能从最基本点开始。只需对酣睡中的动物或人进行体检,我们现在就能说出他是否在做梦。进一步说,我们可以在一秒钟时间内确定他开始做梦的时刻与结束做梦的时刻。”



    “对这一发现,我们有三条基本的生理学原则,现在已被所有的神经生理学家接受:

    1.肌肉紧张性几乎完全消失。


    2.似乎没有目的的快速眼动(因此而产生了快速眼动睡眠这一术语)。


    3.脑电图上特有的脑电波,与酣睡中记录下来的脑电波完全不同,而与醒着时记录下来的脑电波很相似。这种脑波图象的发现导致了“反常阶段”这一术语的出现,这一阶段是指睡梦状态。



    “我们还可以说,一般成人睡眠时间的20%是在做梦,是一系列分开的梦。每一段梦大约延续20分钟,接着是一阵酣睡,以典型的长波显示在脑电记录上。




    “谈到统计数据,我们可以补充说,新生婴儿比成人梦得更多
——占50%的睡眠时间——这一数据适应于所有哺乳动物。



    “我还要指出,做梦的能力不是所有动物种类的属性。在演变量表上先是鸟类具有这一能力,并且只是在有限的程度上
——占它们睡眠时间的0.5%。对爬行动物与两栖动物(如龟类)的所有研究结果都是否定的——它们的睡眠中没有梦境。




    “这是对最新发现的概述,这些发现使我们能详细研究至今令神经生理学家们苦恼的梦的现象以及做梦的基本功能等问题。我们确信,梦担负着一种重要的生理作用,尽管我们还说不出这一作用到底是什么。





    一只孤独的猫蜷缩在小水池中央的一块砖头上,正安详地入睡,同时有一台脑电图仪记录着它的脑波。“我们不让它做梦,”儒弗博士说,“我刚刚解释了,公认的有关动物梦境阶段的生理学标准之一是肌肉紧张性的消失。这只猫可以在砖头上睡觉,但它一开始做梦,肌肉紧张性就消失,它就掉进水中。这使它立即醒过来,爬回到砖头上,舔了舔自己又睡着了
——但他一开始做梦,就又掉进了水里。





    “如果我们把这一实验持续一星期,然后将它放回笼子,我们观察到它非常需要做梦,会将睡眠时间的40%或更多而不仅仅是20%用来做梦。它神经系统的某些地方存在着一种补偿性机理。




    “由于这个原因,我们认为,做梦不是神经系统进入自由运转时出现的毫无意义的现象,它反映了大脑的特定活动,构成某一过程的必然部分。至于这一过程是什么,我们正在探索。



    “近来,我们在确定对伴随着睡梦活动的现象负责的神经中枢位置方面,取得了很大的进展。开始时,我们为了观察它们睡眠行为中的任何干扰,不得不进行外科方面的猜测性工作,相继去掉实验动物脑干的不同部分。



    “睡眠本身是一种高度复杂的现象,那时还没有确定是否存在一种负责睡眠的大脑中枢,或者说对醒觉中枢的简单抑制是否是引起睡眠的原因。
    “然而,我们已成功地、精确地确定了一些中枢的位置,这些中枢负责睡梦活动中的两个主要特点:第一,快速眼动,我们称之为阶段现象,第二,肌肉紧张性的阻塞,我们称之为紧张性现象。



    幻觉状态中的猫

   “这两个中枢加在一起大约有一粒豌豆大。它们相距很近,但我们可以随意采用不同技术来影响其中的一个。控制肌肉紧张性的中枢不到一粒葡萄核大,却使睡梦现象逼真。肌肉紧张性的严重阻滞不再有效,以致睡梦中的动物做出与它梦境中行动一致的各种运动。一位天真的旁观者可能会有这样的印象,认为他是完全醒着并且可能是危险的,但实际上,他的任何行动或动作都与他行走其中的外部世界不相一致。他在睡眠,而他只是按照头脑中闪现的幻想行动。他活在一个虚幻的世界——他在产生幻觉。








    “一旦他醒来,他的行为将变得十分正常。

    在这一实验中,你可以体味到这个中枢的重要性:它在梦中的作用是原生性的。对这些幻觉状态与某些精神疾病之间潜在的相互关系的研究现已取得了进展。



    你也许会认为,梦游可能是这一中枢功能失调所致,但近来实验显示,这一现象不是在做梦的的过程中发生而是在半醒时发生。在睡眠的这个层次
——不是在做梦期间——人们还可以谈话。



    “另一个相关的问题是,宇宙飞行中经历的失重现象是否可能对宇船员产生出乎意料、令人不快的影响,以致于它能产生一种类似于肌肉紧张性消失的状态。入选参加美国人计划的首次月球旅行的内科医生就是一名睡眠专家,这并非巧合。





    做梦可以随意调节

    “但是,生物化学对有关梦的研究将可能导致最为惊人的结果,为我们提供最大胆设想的机会。在过去几年中,化学在生物现象研究中占据稳固的地位。




    “大脑的神经元介质过程激起了目前研究人员极大的兴趣,他们期望在这些过程中找到解决最复杂现象的答案。


    “以海顿为例,他的研究充分地表明,生物化学能为象记忆这样复杂的生物现象开拓新的视角。我们对做梦的研究也同样如此。似乎是处在睡眠的做梦阶段开始时的快速眼动,却可以受到化学抑制剂或先兆的堵塞或扩大。换言之,采用具体的药物,可以完全剥夺动物的梦境,或者把做梦的时间增加到睡眠时间的60%。




    “我只能提供一种指引我们研究的假设。虽然以我们目前的知识状态还难以证明这一假设,但到目前为止还没有与之相抵触的事情。这一假设是:做梦这一活动与神经系统的其它活动不可分离。不存在分开的醒着、睡眠、梦境状态;这些现象构成了某些动物特有的连续体。在醒着状态下,我们的神经系统,特别是大脑,意识到一定数量的感觉,并且通过合成某些具体蛋白质的分子,以化学形式来记录或记忆这些感觉。这种合成在一种高度复杂的过程中进行。





    “新的信息转换成代码化学图式不是即刻的。我们大脑中的化学工厂需要时间,按照某种有待确定的规则,对信息进行储存、选择以及分类。我们可以说,醒着的状态等于在口述录音机上录信息;在深睡时,这一信息被打印出来;在做梦的过程中,每一页或每个句子,或甚至每一个字都被分类并与以前的信息一起存入档案柜,以前的信息是根据精确的、预先确立的规则储存起来 。





    “这能够解释,为什么我们的梦包含了大量的与醒着状态下接收的印象相一致的意象,或者说为什么有些信息被完全扭曲或符号化。白日发生的事件在梦中的合成可能暗示出一种信息“研制剂”,以及对前面已分类和编码的信息的回顾。



    “这一假设还将解释,为什么新生婴儿及幼小动物做梦时间的比例高
——高达成人的两倍以上。



    “我必须承认,尽管这一假设把梦与学习及记忆力联系起来,它却面临着一系列困难。它不能解释为什么这一功能突然在鸟类演变的过程中出现,在哺乳动物那里爆炸性地扩大了。


    “我们必须等一些年,让神经心理学家进一步实验,并对它们进行解释;但有一点似乎已经成立,梦已永远离开非现实的世界,走向了实验室的世界。

 

    

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Text 2

Mind over Time

by Mark Caldwell

 

    Suppose you could reset the inner clocks that run your life — programming yourself, for example, to wake up fresh and alert at 5:30 AM if you had to make a crucial breakfast meeting, or shutting off the hunger that drives you to swallow a bag of tortilla chips every afternoon. If the prospect of controlling your body's timers seems a pleasing luxury, consider the case of Jason K., a New Jersey attorney. Jason suffers from a weakening malfunction of his biological clock called seasonal affective disorder, or SAD. It may seem a remote or even a fanciful ailment, especially during the summer, when its effects ebb, but it can throw the entire year, not to mention a whole life, into terrible turmoil. 

    "It came up on me gradually, over time," Jason says. As the days got darker and darker going into fall and then winter, "My mood got darker. By winter I'd feel an overall sluggishness that made the work difficult; it took dramatically more effort to get anything done. Sleep wasn't restful; I found myself waking up 15 minutes every night just to see what time it was. And I developed an excessive craving for sweets." 

    Jason's experience is not uncommon. In a recent New York City survey, more than one-third of responding adults reported at least mild winter malaise; 6 out of 100 reported severe depression. Michael Terman, a clinical psychologist at New York State Psychiatric Institute in New York City, and a leading SAD researcher, notes that the degree of suffering goes well beyond typical holiday blues. 

    "When it hits," Terman says, "it's not just a matter of mood. It can be truly disabling for five months of the year, and it can cause an active social withdrawal—mothers who can't mother, a loss of interest in work, a total loss of libido." Although the pall usually lifts during the spring, he says, SAD can throw life permanently off course: "It's no small thing if you can't maintain a nine-to-five work schedule in winter." Some SAD sufferers, he says, simply gravitate toward a lifestyle that accommodates the disease. "They tend to drift into work subcultures. They become freelancers, theater people, perennial graduate students—and many end up feeling their early goals in life are unachievable." 

    Yet the syndrome is only one among a constellation of sleep disorders and related ills caused by the malfunctioning biological clocks. Indeed, inner clocks can sometimes cause trouble even when they're ticking away smoothly. The bleary-eyed miseries of jet lag are a familiar example of what can happen when you're hurled across time zones and your personal clock bumps out of sync with the pace of the rest of the world. These are only the obvious disorders. Susceptibility to pain, for example, tends to crest in the morning and ebb as the day wears on. Heart attacks are most likely to strike in midmorning. And biological rhythms can stretch across months as well as days and weeks: many animal species migrate and mate only according to strict seasonal timetables.

    Folklore and common sense have been telling us for centuries that we depend on inner clocks, but what and where they are and how they work had long remained a mystery. Now, thanks to a series of recent laboratory coups, the once-baffling components of our biological clocks have become clearer. For the first time, scientists have a diagram, remarkable in both elegance and simplicity, that shows where in our brains the timer is, how it uses the machinery in our cells as clockwork, and how─like the clacking and jangling Baby Bens that once regulated the pace of American days—it can be slowed down, speeded up, or reset. Most recently researchers have divined how the brain's clock can switch on and turn off pieces of biological machinery, suggesting that we may ultimately be able to regulate these processes at our pleasure, instead of submitting unreliably to their regulating us.

    In the brain, a recently discovered cluster of nerve cells called the suprachiasmatic nucleus, or SCN, appears to be at the heart of timekeeping. In mammals, the organ is remarkably reliable: even if it's removed from an experimental animal and placed in a dish, it can continue to keep time on its own for at least a day. The SCN is actually a pair of structures, like most parts of the brain. One half sits in the left hemisphere and one in the right, just behind and a bit below the eyes. "Each is made up of about 10 000 densely packed neurons," explains Steven Reppert, the Harvard neurobiologist whose laboratory has been a key player in recent discoveries. "The SCNs are located just above where your optic nerves come together at the base of the brain." This is no accident: the SCN depends on light for what circadian-clock experts call entertainment—synchronizing the inner clock with the cycles of light and darkness in the world outside. Some of the latest research, on mice, suggests that mammals have a set of special photoreceptors in their eyes, which pick up light signals and carry them directly to the SCN. These photoreceptors are different from the rods and cones used to perceive light hitting the retina.

    A flood of light striking the right photoreceptors at the right time does just what the knobs on the back of that vintage Baby Ben do: reset the hands of the clock. A burst of light in the morning sets the clock ahead; a burst in the evening puts it backward. If, like Jason, you're a northerner, your inner clock may run slow in winter, falling behind without early-morning light that would normally nudge it forward. "When I talk with patients here in New York," Terman explains, "I tell them that, biologically speaking, they're living in Chicago." When the bedside alarm goes off, New York wakes up, slipping into high gear. But their inner timers lag an hour or more behind, at Chicago or even California time, insisting that their brain and bodies should still be sound asleep.

    Not everyone has the problem. Most people aren't as vulnerable to a lack of morning light, which helps keep the inner clock in tune with the external environment. Every morning, the light of dawn makes its way to the SCN and advances the inner clock, allowing it to catch up with local time, rousing and easing us into daytime activity in blissful synchrony with local time. And because the nerve pathway from the eyes into the SCN bypasses those parts of the brain that register conscious sight, the inner clock can react to ambient light even when we're sound asleep. The light of dawn penetrates the eyelids, registers on the retina, and relays a silent signal into the SCN. If the internal clock has a tendency to run slow, morning light automatically shifts it ahead, putting it back in step with the world outside. It's beautifully simple—unless you live far enough above the equator so that in winter you're up, breakfasted, and at work before dawn. In fact, SAD seems to be more common in northern latitudes. When natural light is scarce, the best way to reset the inner clock is with a burst of artificial light.

    The vital importance of the SCN as a biological time setter is a recent discovery, though not a new one. While its roots go back to the early 1900s it wasn't characterized until the early 1970s. What's really new is an understanding of the SCN's internal mechanism. Neuroscientists have begun to pry off the clock's cover to get a look at the workings. Research at a number of laboratories has revealed the workhorse of the biological clock to be an ingenious and ingeniously simple device in the individual cells that make up the SCN (and perhaps other time-sensitive organs as well). Such cells seem to run the whole system from the bottom up. "We're now pretty certain," Reppert says, "that the SCN is made up of numerous autonomous clocks in individual cells—and all the molecular machinery you need seems to reside in a single neuron." Underneath it all is one clock, the clock in the cell. 

    The clocks are self-starting and remarkably reliable. Even when cut off from eternal light and temporary cues that reveal the time of the day, they slip out of alignment only gradually. Ambient light doesn't control the clocks; it simply helps adjust them.

    Although we're still uncertain how a malfunctioning biological clock affects behavior, or how it can lead to weakening cycles of gloom and anguish, Reppert's team has just published a paper suggesting an answer. They established a connection between the individual nerve cells whose microscopic inner machinery drives the SCN mechanism, and the manufacture of the hormones. The same proteins that built up and break down over a 24-hour cycle to run the circadian clock directly cause the release of a hormone that can regulate how animals act. "Basically, we had a framework for the molecule gears of the circadian clock in mammals," Reppert says, "What we wanted to get was a link to actual behavior."

    Reppert found that clock proteins switch on and off the gene that produces vasopressin. Outside the brain, vasopressin is important in controlling the salt and water balance in the body. In the brain, however, it's practically a different hormone, implicated in cycles of rest and activity in mammals. While vasopressin doesn't seem to influence the kinds of behavior involved in seasonal affective disorder, it does supply an exciting model for a-to-z operation of biological clocks and for how a malfunction can cause abnormalities in mood or behavior. Now scientists can see a continuum from the cycling of light and dark in the atmosphere around us, the world clock, inward to the SCN personal clock, then still further inward to the microscopic nerve-cell clocks, and finally, to the production of a hormone.

    That is only a beginning. Vasopressin is just one of a vast range of substances that regulate behavior. Cellular clocks haven't yet been directly linked to the cycling of familiar behavior- and mood-modulating substances like serotonin and melatonin. "It's going to take another decade to work out a connection between Reppert's work and therapeutics," Terman predicts. But it isn't hard to foresee how visionary circadian-clock therapies might work. As a matter of fact, a couple are already in place. Jet lag, for example, might respond favorably to melatonin, at least for some people. And there's also an effective treatment for SAD. In 1980, Alfred Lewy, at the Oregon Health Sciences University's Sleep and Mood Disorders Laboratory, successfully relieved a man who suffered from recurrent winter depression simply by exposing him to bright light over several days, from six to nine every morning and four to seven every evening. In later treatments Lewy worked the dosage down to two hours of exposure a day at an intensity of 2 500 lux, which approximates the strength of natural light just after the sun has fully risen. Today, standard therapy for SAD patients involves exposure to artificial light for 30 minutes each morning at an intensity of 1 000 lux (which approximates the strength of natural light about 40 minutes after sunset.)

    Terman's group has been working on refining the treatment: a computerized light system for the bedroom, imitating the gradual, naturally intensifying light of dawn. Jason tried it, and it worked beautifully. "Over a couple of hours it simulates the sun coming up," he says. "Somehow you're aware of it even when you're asleep: the light coming through your eyelids is a luxurious feeling." Within days, Jason's depression dissipated, his sleep habits returned to normal, and the sweet tooth cravings became somewhat less pronounced. 

    The possibilities raised by the discoveries on the workings of the biological clock go beyond moodiness and depression. If heart attacks happen at the prompting of a time signal, for example, is there a way to turn that signal off? Is there a way to control weight by spacing out the timing of hunger pangs? Is it possible to predict, even control, not just the day, but the hour, a baby is born? For the first time, science knows where and how to look for the answers to these questions.


(2057 words)  TOP

 

课文二

大脑与时间

马克·卡德威尔

 

    假定你可以重新设置控制你生命的内在之钟——比如,让自己在早晨5点30醒来并且感到精力充沛,反应敏捷,因为你得赴一次重要的早餐约会,或者解除每天下午驱驶你吞下一袋玉米粉圆饼片的饥饿。如果控制身体时钟的前景似乎是令人愉快的享受,那么让我们看一看新泽西州的律师杰生·K的情况。杰生患有生物钟功能失调,称为周期性情感失调症,或SAD。当症状减轻时,特别是在夏天,这似乎是一种遥远的甚至是想像出来的疾病,但它可以使整个一年,暂且不说整个一生,陷入可怕的混乱。





    “它是渐渐降临到我头上的,”杰生说。随着秋天,然后是冬天的来临,天色越来越暗,“我的情绪也变得更加忧郁。到冬天我感到呆滞,工作困难;得付出多得多的力气来完成任何事情。无法安睡;我发现自己每天晚上每隔15分钟就醒来一次,看看时间。我渐渐嗜糖成癖。”



    杰生的经历并非罕见。在纽约市最近的一次调查中,三分之一以上的成人参与者报告自己至少患有轻微的冬季抑郁症;100人中有6人报告了严重的抑郁症。麦克尔·特曼是位于纽约市的纽约州精神病学院的临床心理学家、周期性情感失调症的主要研究者,他指出这种病痛苦的程度超过典型的假日忧郁症。



    “当它发作的时候,”特曼说,“这不只是情绪问题。它能真的使人一年有五个月丧失能力,它可以导致主动逃避社会
——母亲不能尽到母亲的责任,对工作失去兴趣,完全丧失性欲。”他说,尽管阴影在春天消失,周期性情感失调症可以使生活永远脱离常轨:“如果冬天你不能遵守9至5点的工作时间表,它就决不是一件小事。”他说,有些周期性情感失调症患者倾向于一种易于滋生这种病的生活方式。“他们倾向于流入工作的亚文化领域。他们成为自由撰稿人,戏剧工作者,长年读书的研究生——许多人最终觉得,自己早年的生活目标是无法实现的。”




    然而,这一症状只是生物钟失调导致的一系列睡眠失调及相关疾病中的一种。的确,内在时钟有时甚至在正常运转时都会引起麻烦。常见的例子是时差反应,眼睛发红、视力模糊,给人带来许多痛苦,往往发生在你被抛到另外的时区而你的生物钟突然与外部世界节奏失调的时候。这些只是明显的失调。例如,对痛苦的敏感往往在早晨达到高潮,随时间的推移而减轻。心脏病最有可能在上午10点左右发作。而且,生物节奏可延续几个月、几个星期或者几天:许多动物种类只是严格的按季节进行迁移与交配。






    多少世纪以来,民俗与常识一直告诉我们,我们依靠内在时钟,但这些时钟什么样子,在那里,怎样起作用,长期以来仍然是一个谜。现在,幸亏有了一系列最新的实验措施,我们生物钟里那些曾令人困惑的零件变得清楚了。科学家们第一次拥有了一幅既高贵又简单的图表,显示大脑中定时器的位置,它怎样使用细胞中的机械装置作为发条,以及怎样像曾经调节过美国白昼节奏、丁当作响的小本钟一样减速、加速,或重新设置。最近的大多数研究者已经领悟到,大脑时钟是怎样来启动或关闭各个生物机械,这说明我们最终能够以自己的愿望来调节这些过程,而不是心存疑惑地服从它们对我们的调节。






    最近在大脑中发现的神经细胞簇,叫做超染色体交叉细胞核,或SCN,它们似乎处在生物钟运转的核心部位。在哺乳动物体内,这一器官十分可靠:尽管把它从实验动物体内摘除,放在碟子里,它仍然可以单独运转至少一天。像大脑中大部分器官一样,超染色体交叉细胞核实际上是一对结构。其中一个位于左脑半球,另一个在右边,刚好在眼睛后面偏下一点的位置。“每一个由大约10000个紧密靠在一起的神经元组成,”斯迪文·雷佩特解释说。他是哈佛的神经生物学家,其实验室在最新发现中起了关键作用。“超染色体交叉细胞核刚好位于大脑基部眼神经汇合处之上的位置”。这并不是巧合:超染色体交叉细胞核依靠光来进行生物钟专家所指的娱乐
——使体内的生物钟与外部世界的昼夜循环同步。最近在老鼠身上进行的研究显示,哺乳动物的眼部有一套特殊的感光器,用于接收光信息并把这些信息直接带到超染色体交叉细胞核。这些感光器与那些用于感知刺激视网膜的视杆与视锥不同。








    一片强光在适当的时刻击在适当的感光器上,相当于老式小本钟后部旋钮的作用。早晨一阵光将时钟推前;晚上一阵光将时钟拿后,如果你像杰生一样是个北方人,你的生物钟可能在冬天运转缓慢,因为缺乏能够使时钟向前的晨光。“当我在这里与纽约的病人交谈时,”特尔曼解释道:“我告诉他们,从生理上说,他们住在芝加哥。”当床边的闹铃响时,纽约已经醒着,进入了正常的运转。但这些人的生物钟则晚一个小时或更长的时间,停留在芝加哥甚至在加利福尼亚的时间上,相信他们的大脑还仍然处在酣睡之中。






    不是人人都有这个问题。大部分人对缺乏晨光不太敏感。这种光有助于生物钟与外部环境保持协调。每天清晨,黎明的光线射向超染色体交叉细胞核,加快生物钟的速度,使它赶上当地时间,唤醒我们轻松地进入白天的活动,与当地时间快乐地同步。而且,因为眼部到超染色体交叉细胞核这段神经路径绕过了大脑中那些记录感知视觉的器官,生物钟甚至在我们深睡时,对周围光线产生反应。黎明时的光线穿过眼睑,记录在视网膜上,将无声的信号传送到超染色体交叉细胞核,如果内在时钟有放慢的倾向,晨光将自动把它向前调整,使之与外部世界的节奏一致。事情十分简单
——除非你住在遥远的赤道上,在冬天你便可以在黎明之前起床,吃早餐和工作。事实上,周期性情感失调症似乎在北纬地区更加普遍。当缺少自然光的时候,调整生物钟最好的方法是使用人造光。








    超染色体交叉细胞核作为生物时间调节者的重要性即使不是一项新的发现,也是最近的发现。尽管其根源可追溯到20世纪初,但直到20世纪70年代才知道它的特点。真正的新东西是对超染色体内在机理的理解。神经科学家们已经撬开生物钟的外壳,开始探索它的功能。许多实验室的研究已显示,生物钟机器是一种精巧而简单的装置,它构成超染色体交叉细胞核的个体细胞(也许还有其它对时间敏感的器官)。这样的细胞从头至尾使整个系统运转。“我们确信,”雷佩特说,“染色体交叉细胞核是由个体细胞中多数自动时钟构成
——你所需要的分子机械似乎居宿在一个单独的神经元之中。”在它下面是一个时钟,这个细胞中的时钟。






    这些钟自己启动,非常可靠。即使切断长期的光和揭示白昼时间的临时信号,它们只是渐渐地滑出队列。周围的光不能控制这些钟,只是帮助调节它们。




    尽管我们还仍然不能确定生物钟功能失调是怎样影响行为的,或者它是怎样导致每况愈下、周而复始的极度精神忧郁与痛苦,雷佩特的小组已经发表了一篇论文来解答这一问题。他们在个体神经细胞与荷尔蒙的生产之间确立了某种联系。个体神经细胞的内部机械极为细小,能驱动超染色体交叉细胞的机理。直接使生物钟运转的24小时循环中建立与分解的同一类蛋白质,能导致一种调节动物行为的荷尔蒙的释放。“基本上,我们曾有一幅哺乳动物生物钟分子运行图,”雷佩特说,“我们曾想要得到的是它与实际行为的联系。”





    雷佩特发现,时钟蛋白质打开与关闭能产生后叶加压素的基因。在大脑之外,后叶加压素对控制体内盐和水的平衡十分重要。然而,在大脑中,几乎是另一种荷尔蒙体现在哺乳动物休息与活动的循环之中。尽管后叶加压素似乎没有影响与季节性精神失调有关的种种行为,但它的确提供了一种令人激动的生物钟完整运行过程以及功能失调是怎样引起情绪与行为反常的模式。从我们周围环境中光明与黑暗的循环,即世界时钟,到超染色体交叉细胞核个人生物时钟,然后再进一步进入微小的神经细胞时钟,最后到产生一种荷尔蒙,在这样一个过程中,科学家现在可以看到一种连续性。






    这只是开始。后叶加压素只是大量调节行为的物质中的一种。细胞时钟尚未直接与血清素和褪黑激素之类的日常行为与精神调节物质发生联系。特尔曼预言,“还得十年才能将雷佩特的研究与治疗学联系起来。”但是不难预见想象的生物钟治疗法会怎样起作用。事实上,有几项治疗方法已经就绪。例如,至少对有些人来说,时差反应对褪黑激素有好的反应。而且,对周期性情感失调症也有一种有效的治疗方法。1980年,阿尔弗雷德·洛威在俄勒岗健康科学大学的睡眠与情绪失调实验室,用简单的方法每天从上午6点至9点及傍晚4点至7点,让病人连续几天接触强光,成功地为一位患有周期性冬季忧郁症的男人减轻了痛苦。在以后的治疗中,洛威将光线照射量减少至2小时,以2500勒克斯的强度进行治疗,这相当于太阳刚刚完全升起时产生的自然光的强度。今天,周期性情感失调症的标准治疗法包括每天上午以100勒克斯的强度(相当于太阳落山后40分钟后自然光的强度)让病人接受30分钟的人工光。











    特尔曼的小组正在改进这一治疗方法:电脑控制的卧室光照系统,模仿黎明时渐渐变强的自然光。杰生试了这种疗法,有了可喜的效果。“在几小时内,它模拟太阳升起的过程,”他说,“不知为什么即使在你睡觉的时刻你也可以意识到它:光线透过眼睑的过程是一种舒适的感受。”几天以内,杰生的忧郁消失了,他的睡眠习惯恢复了正常,而且他想吃糖的欲望也不那么强烈了。




    关于因生物钟功能的种种发现而增加的医疗上的可能性,已超出了单纯治疗情绪低落和忧郁。例如,如果心脏病发作时发出了时间信息,是否有办法将这一信息停止下来?是否有方法通过分隔饥痛的时间选择来控制体重?是否能够以小时而不是天为单位来预测、甚至是控制婴儿的出生?科学第一次懂得了在哪里以及怎样找到这些问题的答案。



 

 


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