Modelling of auditory evoked potentials of human sleep-wake states.

The shape of evoked potentials is influenced by the level of vigilance, varying with sleep-wake states. In this paper the shape of auditory evoked potentials is modelled by taking two factors, both modulating the underlying neuronal substrate, into account: 'sensory gating' and 'neuronal firing mode'. Under low levels of vigilance sensory gating reduces the amount of neuronal activity reaching the cortical centres. Due to a rise in hyperpolarisations of thalamocortical neurons associated with an increasing depth of sleep, stimulus evoked primary and secondary excitations, seen as correlates of the N1 and N2 waves of the evoked potential, become smaller. Heightened hyperpolarisations also change the spontaneous activity of neurons from the 'tonic' firing mode of wakefulness into the 'burst-pause' firing mode of sleep. The large P220 complex together with the N350 and N550 waves in sleep are caused by the stimulus induced triggering of pauses and bursting of neurons. The results of this modelling experiment confirm the view that sleep-specific components such as P220, N350 and N550 are waves that facilitate and protect sleep, whereas the wake-specific components N1, P2-P3 and N2 have perceptual-cognitive functions. In particular the wake P2-P3 wave is sensitive to cognitive functions, such as attention. Based on the modelling results it is suggested that component negativities, expressed in N1, N2 and N350, reflect excitatory processes, whereas positivity in P2-P3 and P220 is a correlate of inhibitory processes. Hence, the large P3 in an attended condition is also interpreted as an inhibitory process suppressing irrelevant information, facilitation the saliency of relevant information.