Behavioural Brain Research 128 (2002) 53 – 59 Research report Effects of waking-auditory stimulation on human sleep architecture Jose L. Cantero a,b, *, Mercedes Atienza a,b , Rosa M. Salas a a Laboratory of Sleep and Cognition, Ada. de Andalucı ´a 16, 1D-Izda., 41005 Seille, Spain b Laboratory of Neurophysiology, Department of Psychiatry, Harard Medical School, 74 Fenwood Road, Boston, MA 02115, USA Received 9 April 2001; received in revised form 31 May 2001; accepted 31 May 2001 Abstract Evidence suggests that sleep architecture is affected by endogenous homeostatic mechanisms as well as by behavioral and sensory demands during the prior wakefulness. Regarding the auditory system, sensory deprivation has shown to drastically modify the sleep structure, stressing the relevance of such sensory system for sleep organization. Changes in sleep architecture following prolonged auditory stimulation during prior wakefulness would provide additional support to this hypothesis. In the present study, auditory stimulation was administered over a 6 h period prior to sleep. Sleep parameters obtained from visual scoring were quantified across the total sleep period, for each sleep cycle, and for the two halves of the night, separately. Results showed that 6 h of waking-auditory stimulation were followed by an increase in the duration of slow wave sleep, a shortening of the latency between slow wave sleep periods, and a longer sleep onset latency as compared with the baseline night. In contrast, REM sleep parameters were unaffected by the pre-sleep auditory stimulation. These results indicate that sleep architecture depends on auditory demands during the prior wakefulness, suggesting that the local neural activation underlying auditory stimulation may trigger brain control mechanisms selectively involved in both the slow wave sleep maintenance and organization. © 2002 Elsevier Science B.V. All rights reserved. Keywords: Slow wave sleep; Auditory load; Sleep regulation; Sensory processing; Humans www.elsevier.com/locate/bbr 1. Introduction The interest in sleep regulation has triggered large number of studies in the last three decades, which have led to several different theories of sleep function. Evi- dence from sleep deprivation [8,12,14], introduction of naps within the wakefulness period [11,40], and manip- ulations of the sleep-waking cycle [2,9,10] has consis- tently supported the notion that an interaction among homeostatic, circadian, and ultradian processes under- lies sleep regulation. According to these studies, the slow wave activity observed in the electroencephalo- gram (EEG) during stages 3 and 4 of NREM sleep is a function of the duration of prior wakefulness, this activity being mainly determined by homeostatic fac- tors, whereas the ratio of REM and non-REM sleep mostly depends on circadian and ultradian factors [7]. Sleep seems to be also determined by salient behav- ioral events during prior wakefulness. Garcı ´a-Garcı ´a et al. [18] showed that different behavioral manipulations in rats during wakefulness, such as immobilization, excess intake of food, or gentle handling, were associ- ated with different sleep architecture and EEG power density patterns. These authors tentatively proposed that clusters of neurons associated with such experi- ences may be activated during wakefulness which, in turn, may evoke the release of specific sleep-inducing molecules, thereby causing different sleep patterns. However, additional mechanisms, such as local neural changes, are not ruled out to be responsible for changes * Corresponding author. Tel.: +1-617-626-9540; fax: +1-617-734- 7851. E-mail address: jose – cantero@hms.harvard.edu (J.L. Cantero). 0166-4328/02/$ - see front matter © 2002 Elsevier Science B.V. All rights reserved. PII:S0166-4328(01)00269-8