SCN controlled circadian arousal and the afternoon "nap zone".

This paper outlines a conceptual model for the regulation of the circasemidian sleep propensity process with emphasis on a possible mechanism of the afternoon "nap zone". It is proposed that the afternoon nap zone is due to increasing sleep propensity after morning wakening (Borb ly's Process-S) being overwhelmed by a light-sensitive SCN-dependent circadian arousal process of the type discovered by Edgar et al., (1993) and currently being identified in its pathways and neurochemistry by Jouvet and colleagues. It is maintained that this arousal process is reflected in the circadian core body temperature pattern, and that under normal entrained conditions the latter does not resemble a sine-wave or skewed sine-wave. Rather it is very asymmetrical in time and somewhat asymmetrical in amplitude. Cosinor type analyses which enforce symmetry in time and amplitude are therefore ill suited to adequately curve-fit the empirical data. The shape of the circadian arousal system was clarified by meta-analyses of data from three laboratories for three conditions: the normal entrained state, the constant routine, and temporal isolation. Under normal entrained conditions for about one-third of the circadian day core body temperature, and therefore the assumed intensity of the circadian arousal system, is below the mesor with the nadir being at about 0500h; and for about two-thirds of the circadian day it is above the mesor with the acrophase on average being at about 2100h. For modeling purposes, the homeostatic process (Process-S) employed the actual data of the Zurich laboratories for night sleep, but altered the equation for the daytime period to ensure an exponential increase after wake-up. Combining these modified processes indicated that the nap zone could be explained, as predicted, by an increasing homeostatic pressure for sleep across the daytime being reversed by the circadian arousal process. This 2-process combination predicted quite well the shape of the entire circasemidian sleep/wake propensity process and can explain the presence of morning sleep inertia without requiring a third process. It would appear that the circadian arousal process can be modified in phase and in amplitude by a number of normal and pathological conditions.