Kavanau J Lee
Department of Organismic Biology, Ecology and Evolution, University of California at Los Angeles, P.O. Box 951606, Los Angeles, CA 90095-1606, USA.
Arch Ital Biol. 2002 Apr;140(2):109-27.
Mentation during sleep states is thought to originate in an activation of brain circuits that encode inherited and experiential memories. Spontaneous degradation of the strengths of synapses occurs in all brain circuits because of "turnover" of molecules essential for synaptic function. In circuits employed frequently during waking, synaptic strengths are refreshed and maintained in their dedicated or functional ranges largely through use, by virtue of activity-dependent synaptic plasticity. In circuits employed infrequently during waking, synaptic strengths are refreshed largely during sleep, by circuit activations induced by spontaneous, self-generated, largely low-frequency brain waves, also by virtue of activity-dependent synaptic plasticity. The outputs of circuits activated during sleep do not necessarily rise to the level of 'unconscious' awareness. Such an absence of awareness of the outputs of individual circuits, that is, an absence of dreaming, is proposed to be the primitive condition in animals that sleep. On the other hand, temporal binding of these outputs is accompanied by the thoughts and perceptions of dreams, which is proposed to be the advanced condition. Linking or serial ordering of otherwise 'static' thoughts and perceptions gives rise to continuous, often narrative and veridical, dreams. In all cases, dream contents are derived from the memories--not necessarily veridical--encoded in the reinforced circuitry. In the absence of synaptic strength refreshments during sleep, synaptic strengths in infrequently used circuits would weaken and the circuits would become incompetent, with their encoded memories degraded or lost. Maintenance of synaptic strengths in infrequently used circuitry during sleep apparently does not always achieve perfection. Weakened synapses begin to occur in circuits in appreciable numbers in children after the age of about 5 years. When these 'incompetent' circuits (with weakened synapses) are activated during sleep, there are minimal influences on dream contents, namely, distortions that make some objects, such as animals, faces, and scenes, unrecognizable. As weakened synapses increase in numbers with age, the numbers of distorted objects in dreams also increase. In adults, people in as many as 80% of dreams may be unrecognizable. Besides the normal weakening of synaptic strengths, some synapses become defective, in consequence of deleterious, adventitious, exogenous influences, for example, radiation. As these faulty synapses accumulate in old memories, activation of circuits incorporating them during sleep leads to dreams with incoherent, bizarre, or impossible contents. The infrequent activation of such old, incompetent circuits in some waking conditions leads to false memories, delusions, or hallucinations.
睡眠状态下的心理活动被认为起源于对编码遗传记忆和经验记忆的大脑回路的激活。由于突触功能所必需分子的“周转”,所有大脑回路中突触强度都会发生自发衰退。在清醒时频繁使用的回路中,突触强度主要通过使用,凭借活动依赖的突触可塑性,在其专用或功能范围内得到更新和维持。在清醒时不常使用的回路中,突触强度主要在睡眠期间通过自发产生的、主要是低频的脑电波所诱导的回路激活,同样凭借活动依赖的突触可塑性得到更新。睡眠期间被激活的回路的输出不一定会上升到“无意识”意识的水平。这种对单个回路输出缺乏意识,即没有做梦,被认为是睡眠动物的原始状态。另一方面,这些输出的时间绑定伴随着梦的思想和感知,这被认为是高级状态。将原本“静态”的思想和感知进行链接或序列排序会产生连续的、通常是叙事性且逼真的梦。在所有情况下,梦的内容都源自强化回路中编码的记忆——不一定是逼真的记忆。如果在睡眠期间突触强度得不到更新,不常使用的回路中的突触强度就会减弱,这些回路就会变得功能失调,其编码的记忆也会退化或丢失。睡眠期间不常使用的回路中突触强度的维持显然并不总是完美的。大约5岁以后的儿童,相当数量的回路中开始出现突触减弱。当这些“功能失调”的回路(突触减弱)在睡眠期间被激活时,对梦的内容影响极小,即出现一些使某些物体,如动物、面孔和场景变得无法辨认的扭曲。随着年龄增长,减弱的突触数量增加,梦中扭曲物体的数量也会增加。在成年人中,多达80%的梦中人物可能无法辨认。除了突触强度的正常减弱外,一些突触会因有害的、偶然的、外部的影响,例如辐射,而出现缺陷。当这些有缺陷的突触在旧记忆中积累时,睡眠期间包含它们的回路被激活会导致梦的内容不连贯、怪异或荒诞。在某些清醒状态下,这种旧的、功能失调的回路很少被激活会导致错误记忆、妄想或幻觉。