Cognitive Neuroscience of Sleep

摘要: Mechanism is at the heart of understanding, and this chapter addresses underlying brain mechanisms pathways cognition impact sleep on these processes, especially those serving learning memory. This reviews current understanding relationship between sleep/waking states from perspective afforded by basic neurophysiological investigations. The extensive overlap neurophysiology memory processes provide a foundation for theories functional link systems. Each states, with its attendant alterations in neurophysiology, associated facilitation important processes. For rapid eye movement (REM) sleep, salient features such as PGO waves, theta synchrony, increased acetylcholine, reduced levels monoamines and, within neuron, transcription plasticity-related genes, cumulatively allow freely occurring bidirectional plasticity, long-term potentiation (LTP) reversal, depotentiation. Thus, REM provides novel neural environment which synaptic remodelling essential to can occur, least hippocampal complex. During non-REM Stage 2 spindles, cessation subsequent strong bursting noradrenergic cells coincident reactivation cortical targets would also increase allowing targeted plasticity neocortex well. In delta orderly neuronal events phase slow wave activity, together high protein synthesis levels, facilitate that convert early LTP long-lasting LTP. Conversely, does not activate immediate genes de novo sleep-unique genetic combined low acetylcholine may serve reduce strength circuits ~50% delta-coincident do appear their waking firing sequence. results manipulation studies, typically total or deprivation, underscore significance phenomenological associations. Finally, implications will be considered larger association specific both depotentiation integrated into mechanistic models cognition.