The hypothesis that a state of hypoarousal upon awakening should lead to a decrease in amplitude and an increase in latency of the N1-P2 components of the Auditory Evoked Potentials (AEPs) as compared to presleep wakefulness levels, was evaluated after two nocturnal awakenings and after the final morning awakening from a 7.5-h night of sleep. The amplitude of the N1-P2 complex was reduced upon awakening as compared to presleep wakefulness levels, but only following the first nocturnal awakening, scheduled after the first 2 h of sleep. This result is interpreted as indicating a link between slow wave sleep amount, mainly present during the first part of the night, and lowered levels of brain activation upon awakening. The reaction times, recorded concomitantly to AEPs, were more sensitive to the negative effects of sleep inertia.