Abstract
This chapter summarizes the current views on the cellular and network mechanisms of three electroencephalogram (EEG) rhythms: the classical posterior alpha rhythm, the theta waves of light non-rapid-eye-movement (NREM) sleep, and the slow (<1 Hz) sleep oscillation. Studying these rhythms is key in achieving a comprehensive knowledge of brain function in health and disease states. The alpha rhythm of relaxed wakefulness and the theta waves of early NREM sleep are mainly driven by thalamic pacemaker units comprising a small number of high threshold (HT) bursting thalamocortical (TC) neurons that are connected by gap junctions and entrain local GABAergic interneurons, and the remaining TC neurons that fire in a classical relay mode, i.e., with a tonic single action potential output. Contrary to the pervading corticocentric view, we believe that the EEG slow (<1 Hz) rhythm of NREM sleep is an emergent property of corticothalamic networks, which originates from the dynamic interplay of three cardinal oscillators: the mainly, but not necessarily exclusively, synaptically based cortical oscillator, and two intrinsic, conditional thalamic oscillators, i.e., TC and nucleus reticularis thalami (NRT) neurons.
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