Homer1a and 1bc levels in the rat somatosensory cortex vary with the time of day and sleep loss

Nelson, Scott E.; Duricka, Deborah; Campbell, Kenneth C.; Churchill, Lynn; Krueger, James M.

doi:10.1016/j.neulet.2004.05.089

Cited by 46 publications

(22 citation statements)

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“…In addition, the activity and neurotransmitterinduced early genes ania-1 and ania-3 (aka homer-1) and early growth response 1 (egr-1; also known as ngfi-a and krox-24) were upregulated in the present study; these genes were also identified as "wake-related" in rat Cx (Cirelli et al, 2004). Other studies have previously found egr-1/ngfi-a/krox-24 to be upregulated in the rodent Cx either during spontaneous wakefulness (Pompeiano et al, 1994) or in response to SD (O'Hara et al, 1993, Terao et al, 2003a and homer-1 to be upregulated in response to SD (Nelson et al, 2004). In addition, levels of arc mRNA, which encodes a cytoskeletal protein associated with activity-dependent synaptic plasticity (Lyford et al, 1995, Guzowski et al, 2000, are high during wakefulness and decrease during sleep (Cirelli and Tononi, 2000b).…”

Section: Affymetrix Genechip ® Studysupporting

confidence: 69%

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

et al. 2006

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Previous studies have demonstrated that macromolecular synthesis in the brain is modulated in association with the occurrence of sleep and wakefulness. Similarly, the spectral composition of electroencephalographic activity that occurs during sleep is dependent on the duration of prior wakefulness. Since this homeostatic relationship between wake and sleep is highly conserved across mammalian species, genes that are truly involved in the electroencephalographic response to sleep deprivation (SD) might be expected to be conserved across mammalian species. Therefore, in the rat cerebral cortex, we have studied the effects of SD on the expression of immediate early gene (IEG) and heat shock protein (HSP) mRNAs previously shown to be upregulated in the mouse brain in SD and in recovery sleep (RS) after SD. We find that the molecular response to SD and RS in the brain is highly conserved between these two mammalian species, at least in terms of expression of IEG and HSP family members. Using Affymetrix Neurobiology U34 GeneChips ® , we also screened the rat cerebral cortex, basal forebrain, and hypothalamus for other genes whose expression may be modulated by SD or RS. We find that the response of the basal forebrain to SD is more similar to that of the cerebral cortex than to the hypothalamus. Together, these results suggest that sleep-dependent changes in gene expression in the cerebral cortex are similar across rodent species and therefore may underlie sleep historydependent changes in sleep electroencephalographic activity. KeywordsTaqman analysis; sleep deprivation; immediate early genes; basal forebrain; cerebral cortex; hypothalamus HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptSleep is a homeostatic process in that the time spent asleep and the continuity of sleep states are directly related to the duration of prior wakefulness. Although sleep duration and the time spent in each of its stages are parameters commonly measured in sleep studies, sleep also has an intensity dimension, measurable by slow wave activity (SWA) in the electroencephalogram (EEG) during non-rapid eye movement (NREM) sleep. The amplitude of EEG SWA is directly proportional to the duration of prior wake and consequently has been proposed as a marker for the homeostatic regulation of sleep in mammals (Borbely and Achermann, 2000). Accordingly, sleep need, measurable as EEG SWA once sleep is initiated, is thought to accrue during wakefulness. Conversely, the decline of EEG SWA amplitude across a sleep bout is thought to reflect the diminution of the sleep-dependent "Process S" that reflects recovery from prior waking activities.The temporal dynamics of the sleep-dependent discharge of sleep need (reflected in the decay of the sleep-dependent Process S) is conserved among genetically distinct rodent strains (Franken et al., 2001). The conserved nature of Process S supports the concept that EEG SWA may be an electrophysiological marker of restorative neurochemical processes that occur during...

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Section: Affymetrix Genechip ® Studysupporting

confidence: 69%

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

et al. 2006

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“…In one study in rats the inhibitory isoform homer1a was found to be upregulated during sleep deprivation (84). A second study, again in rats, found that although both homer1a and homerbc isoforms were upregulated during sleep deprivation, homer1a was significantly more upregulated than the homerbc isoform (64). Downregulation of homer in the fly or upregulation of homer1a in the rat with sleep deprivation would result in the same outcome, a less effective coupling of Fig.…”

Section: Resultsmentioning

confidence: 98%

Multiple mechanisms limit the duration of wakefulness in Drosophila brain

Zimmerman

Rizzo

Shockley

et al. 2006

Physiological Genomics

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.-The functions of sleep and what controls it remain unanswered biological questions. According to the two-process model, a circadian process and a homeostatic process interact to regulate sleep. While progress has been made in understanding the molecular and cellular functions of the circadian process, the mechanisms of the homeostatic process remain undiscovered. We use the recently established sleep model system organism Drosophila melanogaster to examine dynamic changes in gene expression during sleep and during prolonged wakefulness in the brain. Our experimental design controls for circadian processes by killing animals at three matched time points from the beginning of the consolidated rest period [Zeitgeber time (ZT) 14)] under two conditions, sleep deprived and spontaneously sleeping. Using ANOVA at a false discovery rate of 5%, we have identified 252 genes that were differentially expressed between sleep-deprived and control groups in the Drosophila brain. Using linear trends analysis, we have separated the significant differentially expressed genes into nine temporal expression patterns relative to a common anchor point (ZT 14). The most common expression pattern is a decrease during extended wakefulness but no change during spontaneous sleep (n ϭ 114). Genes in this category were involved in protein production (n ϭ 47), calcium homeostasis, and membrane excitability (n ϭ 5). Multiple mechanisms, therefore, act to limit wakefulness. In addition, by studying the effects of the mechanical stimulus used in our deprivation studies during the period when the animals are predominantly active, we provide evidence for a previously unappreciated role for the Drosophila immune system in the brain response to stress. sleep deprivation; temporal regulation; stress SLEEP HAS BEEN OBSERVED in animal species ranging from insects to humans. We know that total sleep deprivation results in animal death (3,69,70), but the biological function of sleep remains poorly understood. With a rising prevalence of sleep restriction in our society (2, 6, 26), it becomes increasingly important to understand the function and regulation of sleep as well as the consequences of sleep deprivation on the brain.A popular conceptual framework to understand the regulation of sleep is called the two-process model. According to this model, a circadian process and a sleep-promoting (homeostatic) process, which are mechanistically distinct, interact to regulate sleep (7,8). While the cellular and molecular basis for the circadian process has been largely delineated, the homeostatic process remains poorly understood. A key feature of the homeostatic process is that the drive for sleep is proportional to the prior duration of wakefulness and that the restorative function of sleep is related to sleep time. Therefore, to understand the molecular underpinnings of the homeostatic process, wakefulness and sleep cannot be treated as single static behavioral states but, rather, as dynamic processes.To gain insight into the dynamic molecular processes th...

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“…The low cortical expression of BDNF during mammalian sleep [30–32] should upscale synapses, because reducing BDNF upscales synaptic strength [7, 33]. The low cortical expression of Arc and Homer1a, during sleep [30, 31, 34] should have similar effects because both molecules normally promote synaptic downscaling via AMPAR endocytosis [35–37]. Tnf α is released at higher concentrations during sleep [38, 39], has a permissive role in synaptic scaling [134], and promotes synaptic strengthening in situ [40] and in vivo [98].…”

Section: The Mechanisms Of Shymentioning

confidence: 99%

Erasing Synapses in Sleep: Is It Time to Be SHY?

Frank

2012

Neural Plasticity

102

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Converging lines of evidence strongly support a role for sleep in brain plasticity. An elegant idea that may explain how sleep accomplishes this role is the “synaptic homeostasis hypothesis (SHY).” According to SHY, sleep promotes net synaptic weakening which offsets net synaptic strengthening that occurs during wakefulness. SHY is intuitively appealing because it relates the homeostatic regulation of sleep to an important function (synaptic plasticity). SHY has also received important experimental support from recent studies in Drosophila melanogaster. There remain, however, a number of unanswered questions about SHY. What is the cellular mechanism governing SHY? How does it fit with what we know about plasticity mechanisms in the brain? In this review, I discuss the evidence and theory of SHY in the context of what is known about Hebbian and non-Hebbian synaptic plasticity. I conclude that while SHY remains an elegant idea, the underlying mechanisms are mysterious and its functional significance unknown.

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Homer1a and 1bc levels in the rat somatosensory cortex vary with the time of day and sleep loss

Cited by 46 publications

References 11 publications

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

Gene expression in the rat brain during sleep deprivation and recovery sleep: an Affymetrix GeneChip® study

Multiple mechanisms limit the duration of wakefulness in Drosophila brain

Erasing Synapses in Sleep: Is It Time to Be SHY?

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