Regional differences in NREM sleep slow-wave activity in mice with congenital callosal dysgenesis VLADYSLAV V. VYAZOVSKIY and IRENE TOBLER Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland Accepted in revised form 30 March 2005; received 27 January 2005 SUMMARY Topographic differences in the sleep EEG have been repeatedly found in humans and rodents. A frontal predominance of EEG slow-wave activity (0.75–4 Hz; delta band) during non-rapid eye movement (NREM) sleep is particularly evident under conditions of increased sleep propensity. Local aspects of neuronal connectivity in the neocortex that are modified by specific neuronal stimulation may underlie these differences. To investigate the role of altered neuronal connectivity on anterior–posterior EEG topography, sleep was recorded in mice with congenital dysgenesis of the corpus callosum (B1 strain) during baseline and after 6 h sleep deprivation (SD). In these mice neuronal connections within a hemisphere are increased due to the longitudinal Probst bundle, a structure of re-routed callosal fibers. After SD the frequencies above 1.5 Hz within the delta band in NREM sleep were reduced in B1 mice compared with control C57BL/6 mice, a strain that has a normal corpus callosum, while power in the lowest frequency band (0.75–1.0 Hz) was enhanced in B1 mice. The differences between the strains subsided in the course of recovery. The redistribution of EEG power within the delta band in the frontal region in mice with a well developed Probst bundle, suggests a role of intracortical connectivity in local sleep regulation. keywords corpus callosum, EEG spectral analysis, local sleep, sleep, sleep home- ostasis INTRODUCTION Slow-wave activity (SWA, EEG power between 0.75 and 4 Hz; delta band) in non-rapid eye movement (NREM) sleep increases proportionally to the duration of previous waking (Borbe´ly, 1982). The level of SWA differs between cortical areas, suggesting that local mechanisms are involved in sleep regulation. Thus in humans and rodents frontal regions respond to increased sleep pressure with a higher initial level of SWA (Cajochen et al., 1999; Finelli et al., 2001; Huber et al., 2000b, 2002; Schwierin et al., 1999; Vyazovskiy et al., 2002; Werth et al., 1996). It has been postulated that sleep is a local use-dependent process (Krueger et al., 1999). This hypothesis is supported by experiments showing that sensory peripheral stimulation during waking leads to regional differ- ences in sleep intensity (Kattler et al., 1994; Vyazovskiy et al., 2000, 2004b). The hypothesis that local enhancement of slow waves may be a result of increased synaptic potentiation induced by preceding waking activity (Tononi and Cirelli, 2003) was supported by high-density EEG recordings in humans after a motor learning task (Huber et al., 2004). Mice with congenital dysgenesis of the corpus callosum (Lipp and Wahlsten, 1992) are particularly suited to investi- gate consequences of altered neocortical connectivity (Vya- zovskiy et al., 2004a). In these mice callosal fibers fail to cross the midline, forming instead a novel structure, the longitudinal bundle of Probst (Ozaki and Shimada, 1988). This structure is most prominent in the rostral portion of the hemispheres and provides redundant ipsilateral cortico-cortical connections (Ozaki and Shimada, 1988; Ozaki and Wahlsten, 1993; Ozaki et al., 1989). This alteration in cortical connectivity might affect the level of synchronization between neurons within the frontal cortical area, as well as between the anterior and posterior cortical areas. If this is the case, congenital callosal dysgenesis should modify regional EEG differences during sleep. We investigated this aspect in mice with a high incidence of callosal dysgenesis (B1, I/LnJ · C57BL/6, Magara, 1999; Correspondence: Prof. Irene Tobler PhD, Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstr 190, CH-8057 Zurich, Switzerland. Tel.: +41 (0)1 635 59 57; fax: +41 (0)1 635 57 07; e-mail: tobler@pharma.unizh.ch J. Sleep Res. (2005) 14, 299–304 Ó 2005 European Sleep Research Society 299