Sleep, clocks, and synaptic plasticity

Frank, Marcos G.; Cantera, Rafael

doi:10.1016/j.tins.2014.06.005

Cited by 104 publications

(109 citation statements)

References 112 publications

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“…Theories for sleep function include roles in brain energetics [1], brain recovery [2], somatic functions and thermoregulation [3], biosynthesis [4], neural plasticity [5,6], and allocation of energetic resources [7]. A key challenge for sleep researchers is to determine whether identified sleep functions are particular to the organism of study, or if they represent core functions that led to the evolutionary maintenance of sleep states.…”

Section: Behavioral and Electrophysiological Properties Of Sleepmentioning

confidence: 99%

Call it Worm Sleep

Trojanowski

Raizen

2016

Trends in Neurosciences

115

109

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The nematode Caenorhabditis elegans stops feeding and moving during a larval transition stage called lethargus and following exposure to cellular stressors. These behaviors have been termed “sleep-like states”. We argue that these behaviors should instead be called “sleep”. Sleep during lethargus is similar to sleep regulated by circadian timers in insects and mammals, and sleep in response to cellular stress is similar to sleep induced by sickness in other animals. Sleep in mammals and Drosophila shows molecular and functional conservation with C. elegans sleep. The simple neuroanatomy and powerful genetic tools of C. elegans have yielded insights into sleep regulation and hold great promise for future research into sleep regulation and function.

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Section: Behavioral and Electrophysiological Properties Of Sleepmentioning

confidence: 99%

Call it Worm Sleep

Trojanowski

Raizen

2016

Trends in Neurosciences

115

109

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“…Cortical activity patterns, sensory drive, modulatory tone, and induction of plasticity all differ between sleep and wake (Frank and Cantera, 2014; Steriade and Timofeev, 2003; Jones, 2005). We showed previously that FR homeostasis restores ensemble average firing when measured during sleep or wake (Hengen et al, 2013), indicating that once homeostatic adjustments have occurred, they serve to stabilize the same network across these distinct internal states.…”

Section: Introductionmentioning

confidence: 99%

“…In contrast, another influential theory about the function of sleep, the sleep replay hypothesis (Abel et al, 2013), is agnostic about when FR homeostasis should occur. Although a number of experiments have been undertaken to test SHY (Frank and Cantera, 2014; Tononi and Cirelli, 2014), the key prediction of this hypothesis – that FR homeostasis triggered by a perturbation to the circuit should occur only during sleep – has never been tested.…”

Section: Introductionmentioning

confidence: 99%

Neuronal Firing Rate Homeostasis Is Inhibited by Sleep and Promoted by Wake

Hengen

Pacheco

McGregor

et al. 2016

Cell

275

366

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SUMMARY Homeostatic mechanisms stabilize neural circuit function by keeping firing rates within a set-point range, but whether this process is gated by brain state is unknown. Here, we monitored firing rate homeostasis in individual visual cortical neurons in freely behaving rats as they cycled between sleep and wake states. When neuronal firing rates were perturbed by visual deprivation, they gradually returned to a precise, cell-autonomous set-point during periods of active wake, with lengthening of the wake period enhancing firing rate rebound. Unexpectedly, this resetting of neuronal firing was suppressed during sleep. This raises the possibility that memory consolidation or other sleep-dependent processes are vulnerable to interference from homeostatic plasticity mechanisms.

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“…Both SHY and the synaptic embossing theory have empirical bases, but the experimental designs of the conflicting studies are not congruent, and therefore a consensus is yet to be established (Diekelmann & Born, 2010;Frank & Cantera, 2014;Tononi & Cirelli, 2014). To properly compare these theories it is necessary to investigate plasticity factors in animals with and without preexposure to novel stimulation.…”

Section: Introductionmentioning

confidence: 99%

Experience-dependent upregulation of multiple plasticity factors in the hippocampus during early REM sleep

Calais

Ojopi

Morya

et al. 2015

Neurobiology of Learning and Memory

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Sleep is beneficial to learning, but the underlying mechanisms remain controversial. The synaptic homeostasis hypothesis (SHY) proposes that the cognitive function of sleep is related to a generalized rescaling of synaptic weights to intermediate levels, due to a passive downregulation of plasticity mechanisms. A competing hypothesis proposes that the active upscaling and downscaling of synaptic weights during sleep embosses memories in circuits respectively activated or deactivated during prior waking experience, leading to memory changes beyond rescaling. Both theories have empirical support but the experimental designs underlying the conflicting studies are not congruent, therefore a consensus is yet to be reached. To advance this issue, we used real-time PCR and electrophysiological recordings to assess gene expression related to synaptic plasticity in the hippocampus and primary somatosensory cortex of rats exposed to novel objects, then kept awake (WK) for 60 min and finally killed after a 30 min period rich in WK, slow-wave sleep (SWS) or rapid-eye-movement sleep (REM). Animals similarly treated but not exposed to novel objects were used as controls. We found that the mRNA levels of Arc, Egr1, Fos, Ppp2ca and Ppp2r2d were significantly increased in the hippocampus of exposed animals allowed to enter REM, in comparison with control animals. Experience-dependent changes during sleep were not significant in the hippocampus for Bdnf, Camk4, Creb1, and Nr4a1, and no differences were detected between exposed and control SWS groups for any of the genes tested. No significant changes in gene expression were detected in the primary somatosensory cortex during sleep, in contrast with previous studies using longer post-stimulation intervals (>180 min). The experience-dependent induction of multiple plasticity-related genes in the hippocampus during early REM adds experimental support to the synaptic embossing theory.

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Sleep, clocks, and synaptic plasticity

Cited by 104 publications

References 112 publications

Call it Worm Sleep

Call it Worm Sleep

Neuronal Firing Rate Homeostasis Is Inhibited by Sleep and Promoted by Wake

Experience-dependent upregulation of multiple plasticity factors in the hippocampus during early REM sleep

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