Feinberg I, March J D
Veterans Administration, Northern California System of Clinics, University of California at Davis 95616, USA.
Behav Brain Res. 1995 Jul-Aug;69(1-2):97-108. doi: 10.1016/0166-4328(95)00010-q.
We first review the concept of delta homeostasis as formulated in our 1974 model and as developed quantitatively by Borbely and colleagues in several versions of the two-process model. We illustrate difficulties in the application of this quantitative model to the negative delta rebound in the rat and we put forward additional evidence that the negative rebound is a pathological rather than a homeostatic response to sleep deprivation. We next review experiments on rats in which the waking metabolic rate of limbic structures was increased by blockade of the NMDA-gated cation channel with ketamine and MK-801. As predicted by the 1974 homeostatic model, NREM delta increased during subsequent sleep. However, it remains to be shown that this powerful effect is actually caused by the metabolic change and that it is an intensification of physiological sleep rather than a non-specific increase in EEG slow waves caused by neurotoxicity. We then outline our one-stimulus model of NREM/REM alternation. In this model NREM sleep is induced by periodic (neuroendocrine?) pulses. These pulses increase delta EEG amplitude and density, depress arousal level and inhibit neural activity. When the strength of the pulsatile stimulus falls below a critical level, REM emerges as neuronal escape. Last, we discuss the neurobiologic implications of two robust findings in experimental dream studies: the relation of dream reports to arousal and the consistent failure of controlled studies to demonstrate qualitative differences between NREM and REM mentation.
我们首先回顾一下1974年模型中提出的以及由博尔贝利及其同事在双过程模型的几个版本中进行定量发展的δ稳态概念。我们阐述了将此定量模型应用于大鼠负δ反弹时所面临的困难，并提出了更多证据，证明负反弹是对睡眠剥夺的一种病理性而非稳态反应。接下来，我们回顾了对大鼠进行的实验，在这些实验中，通过用氯胺酮和MK - 801阻断NMDA门控阳离子通道来提高边缘系统的清醒代谢率。正如1974年稳态模型所预测的，随后睡眠期间非快速眼动（NREM）δ波增加。然而，仍有待证明这种强大的效应实际上是由代谢变化引起的，并且它是生理性睡眠的增强，而非由神经毒性导致的脑电图慢波非特异性增加。然后，我们概述了我们的NREM/REM交替单刺激模型。在这个模型中，NREM睡眠由周期性（神经内分泌？）脉冲诱导。这些脉冲增加δ脑电图的振幅和密度，降低唤醒水平并抑制神经活动。当脉动刺激的强度降至临界水平以下时，快速眼动（REM）作为神经元逃逸出现。最后，我们讨论了实验性梦境研究中两个有力发现的神经生物学意义：梦境报告与唤醒的关系以及对照研究一直未能证明NREM和REM思维之间存在质的差异。
