Abstract

Certain features of Stage NREM sleep – for example, rhythmic voltage oscillation in thalamic neurons – are physiologically inhospitable to “REM sleep processes.” In Stage 2, the sleep spindle and its refractory period must limit the incursion of “covert REM,” and thus the extent of REM-like cognition. If these hyperpolarization-dependent events also inform Stage NREM cognition, does a “1-gen” model suffice to account for REM-NREM differences? [Nielsen].