| The slow (<1 Hz) rhythm, the most significant EEG feature of non-NREM sleep, is generally viewed as originating exclusively from neocortical networks. In my presentation, I will argue that this rhythm should no longer be viewed as originating solely from cortical regions, but from the intricate dynamic interactions of three independent oscillators: a predominantly, but not exclusively, synaptically-based cortical oscillator and two intrinsic, conditional thalamic oscillators. In particular, the prominent LTCP-mediated bursts that initiate the UP states in TC neurons provide an ideal signal for initiating large-scale UP states in cortical networks. I will also discuss how the gradual increase in slow wave frequency that occurs as sleep or anesthesia are deepened and the conserved waveform of individual slow waves, or K-complexes, can only be satisfactorily explained by considering the intrinsic oscillatory properties of individual thalamic neurons. As well as fully accounting for the available data, this scenario also allows novel interpretations regarding the intricate cross-talk between thalamus and cortex which may ultimately have profound implications for understanding the functional relevance of NREM sleep. |
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