Thalamus and cortex: inseparable partners in shaping sleep slow waves?

Editor's Note: These short, critical reviews of recent papers in the Journal, written exclusively by graduate students or postdoctoral fellows, are intended to summarize the important findings of the paper and provide additional insight and commentary. For more information on the format and purpose of the Journal Club, please see Review of Lemieux et al. Sleep slow waves have gained increasing attention since the pioneering work of Steriade et al. (1993a,b) unraveled their underlying cellular mechanism, i.e., the slow (Ͻ1 Hz) and sometimes rhythmic alternation of the membrane potential between depolarized (up) and hyperpolar-ized (down) states. Since then, it has been discovered that slow waves can emerge in cortical and subcortical brain areas (Crunelli and Hughes, 2010), and it has been proposed that they have important roles in the consolidation of memory (Marshall et al., 2006). In vitro studies (Sanchez-Vives and McCormick, 2000; Crunelli and Hughes, 2010) have identified some of the ionic and synaptic mechanisms critical for the emergence of slow oscillations at both the cortical and thalamic levels. However, how in vivo network mechanisms generate the often dynamic and complex physiology of sleep slow waves remained largely elusive. How can slow waves be either local or generalized across brain areas? Why do their frequency and regularity vary? Is there only one site of initiation , and if so where? The recent study by Lemieux et al. (2014) bridges the gap between theories attributing an exclusive origin of slow waves to the cortex (Steriade et al., 1993b; Sanchez-Vives and McCor-mick, 2000) and contradictory observations involving other structures, especially the thalamus (Crunelli and Hughes, 2010; Da-vid et al., 2013). In Steriade et al.'s (1993b) early work on the cellular mechanisms of the slow oscillation (and slow waves), a crucial experiment suggested that the thalamus did not play a role in the generation or upkeep of the slow oscillation: recordings performed in cats 2 d after the thalamus had been lesioned still revealed robust slow oscillations in cortex. This was reinforced by later experiments in vitro in cortical slices and in vivo in cortical slab (i.e., a deaffer-ented piece of cortex maintained in situ), which showed that some of the main dynamic features typical of slow oscillations were still present in these isolated pieces of cortex (for review, see Crunelli and Hughes, 2010). In the same species and under similar anesthesia as in Steriade et al. (1993b), but contrary to the …