In the mammalian brain, sleep and wakefulness are associated with widespread changes in gene expression. The extent to which the molecular correlates of vigilance state are conserved across phylogeny, however, is only beginning to be explored. The goal of this study was to determine whether sleep and wakefulness affect gene expression in the avian brain. To achieve this end we performed an extensive microarray analysis of gene expression during sleep, wakefulness, and short‐term sleep deprivation in the telencephalon of the white‐crowned sparrow (Zonotrichia leucophrys gambelii). We found that, as in the rodent cerebral cortex, behavioral state, independent of time of day, has widespread effects on avian brain gene expression, affecting the transcript levels of 255 genes (1.4% of all tested transcripts). Wakefulness‐related transcripts (n = 114) code for proteins involved in energy metabolism and oxidative phosphorylation, immediate early genes and transcription factors associated with activity‐dependent neural plasticity, as well as heat‐shock proteins and molecular chaperones associated with the unfolded protein response. Sleep‐related transcripts (n = 141) code for proteins involved in membrane trafficking, lipid/cholesterol synthesis, translational regulation, cellular adhesion, and cytoskeletal organization. Remarkably, despite the considerable differences in morphology and cytology between the mammalian neocortex and the avian telencephalon, the functional categories of transcripts identified in this study exhibit a significant degree of overlap with those identified in the rodent cortex.

This investigation suggests that regional deficits in electroencephalography (EEG) power generation may be a useful clinical marker for neural disruption in obstructive sleep apnea, and that high-density EEG may have the sensitivity to detect pathological cortical changes early in the disease process.

BackgroundSleep is regulated by both a circadian and a homeostatic process. The homeostatic process reflects the duration of prior wakefulness: the longer one stays awake, the longer and/or more intense is subsequent sleep. In mammals, the best marker of the homeostatic sleep drive is slow wave activity (SWA), the electroencephalographic (EEG) power spectrum in the 0.5–4 Hz frequency range during non-rapid eye movement (NREM) sleep. In mammals, NREM sleep SWA is high at sleep onset, when sleep pressure is high, and decreases progressively to reach low levels in late sleep. Moreover, SWA increases further with sleep deprivation, when sleep also becomes less fragmented (the duration of sleep episodes increases, and the number of brief awakenings decreases). Although avian and mammalian sleep share several features, the evidence of a clear homeostatic response to sleep loss has been conflicting in the few avian species studied so far. The aim of the current study was therefore to ascertain whether established markers of sleep homeostasis in mammals are also present in the white-crowned sparrow (Zonotrichia leucophrys gambelii), a migratory songbird of the order Passeriformes. To accomplish this goal, we investigated amount of sleep, sleep time course, and measures of sleep intensity in 6 birds during baseline sleep and during recovery sleep following 6 hours of sleep deprivation.ResultsContinuous (24 hours) EEG and video recordings were used to measure baseline sleep and recovery sleep following short-term sleep deprivation. Sleep stages were scored visually based on 4-sec epochs. EEG power spectra (0.5–25 Hz) were calculated on consecutive 4-sec epochs. Four vigilance states were reliably distinguished based on behavior, visual inspection of the EEG, and spectral EEG analysis: Wakefulness (W), Drowsiness (D), slow wave sleep (SWS) and rapid-eye movement (REM) sleep. During baseline, SWA during D, SWS, and NREM sleep (defined as D and SWS combined) was highest at the beginning of the major sleep period and declined thereafter. Moreover, peak SWA in both SWS and NREM sleep increased significantly immediately following sleep deprivation relative to baseline.ConclusionAs in mammals, sleep deprivation in the white-crowned sparrow increases the intensity of sleep as measured by SWA.

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Long-term recordings of seasonal sleep patterns in captive white-crowned sparrows (Zonotrichia leucophrys gambelii) have shown that these birds markedly reduce sleep time during the migratory period relative to the non-migratory period. It was also found that, despite this sleep reduction, sparrows showed no evidence of neurobehavioral deficits in a standard operant task used to assess the effects of sleep loss. In this study, we performed an extensive microarray analysis of gene expression in the sparrow telencephalon during the migratory season (M), relative to a 78-hour period of enforced sleep restriction during the non-migratory season (SR), and a 6-hour period of normal wakefulness during the non-migratory season (W). Of the estimated 17,100 transcripts that were reliably detected, only 0.17% changed expression as a function of M (relative to both SR and W), and 0.11% as a function of SR (relative to both M and W). Brain transcripts whose expression increased during M include the facilitated glucose transporter GLUT1, the presenilin associated rhomboid-like protein PARL, and several members of the heat shock protein family, such as HSP70, HSP90, GRP78 and BiP. These data suggest that migration is associated with brain cellular stress and enhanced energetic demands.