[Show abstract][Hide abstract] ABSTRACT: A comprehensive review is presented of reported aspects and putative mechanisms of sleep-like motility rhythms throughout the animal kingdom. It is proposed that 'rapid eye movement (REM) sleep' be regarded as a special case of a distinct but much broader category of behavior, 'rapid body movement (RBM) sleep', defined by intrinsically-generated and apparently non-purposive movements. Such a classification completes a 2 × 2 matrix defined by the axes sleep versus waking and active versus quiet. Although 'paradoxical' arousal of forebrain electrical activity is restricted to warm-blooded vertebrates, we urge that juvenile or even infantile stages of development be investigated in cold-blooded animals, in view of the many reports of REM-like spontaneous motility (RBMs) in a wide range of species during sleep. The neurophysiological bases for motorically active sleep at the brainstem level and for slow-wave sleep in the forebrain appear to be remarkably similar, and to be subserved in both cases by a primitive diffuse mode of neuronal organization. Thus, the spontaneous synchronous burst discharges which are characteristics of the sleeping brain can be readily simulated even by highly unstructured neural network models. Neuromotor discharges during active sleep appear to reflect a hierarchy of simple relaxation oscillation mechanisms, spanning a wide range of spike-dependent relaxation times, whereas the periodic alternation of active and quiet sleep states more likely results from the entrainment of intrinsic cellular rhythms and/or from activity-dependent homeostatic changes in network excitability.
[Show abstract][Hide abstract] ABSTRACT: Our knowledge of cytokine sleep mechanisms has led to a view of brain organization of sleep positing that sleep is a local property of neural networks. Cortical columns oscillate between functional states; the sleeplike state of cortical columns is promoted by multiple cytokines. Cytokine-mediated sleep mechanisms support the hypothesis that sleep serves a synaptic- connectivity function and is tightly coupled to cerebral metabolism. Cytokine release from glia is enhanced by neuronal activity via adenosine triphosphate signaling and, in turn, these cytokines activate nuclear factor κ B, adenosine, and other downstream mechanisms thereby linking activity to local changes in state.
Sleep Medicine Clinics 09/2012; 7(3):517–527. DOI:10.1016/j.jsmc.2012.06.006
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