Local sleep and learning

Huber, Reto; Ghilardi, Maria Felice; Massimini, Marcello; Tononi, Giulio

doi:10.1038/nature02663

Cited by 1,660 publications

(1,497 citation statements)

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“…Firstly, decreased activity in the parietal lobes has been consistently reported in relation to enhanced motor skill learning (Seitz et al, 1990;Toni et al, 1998;Muller et al, 2002), a phenomena believe to reflect improved sequence automation. Secondly, Huber et al (2004) recently reported that daytime learning of a motor adaptation task results in a discrete increase in the subsequent amount of NREM slow-wave activity over the parietal cortex, and that this slow-wave increase was proportional to the amount of delayed learning that developed the next day; signifying a potential link between overnight plastic changes in the parietal cortex and the degree of sleep-dependent improvement. Supporting these findings, and based on our current results, we hypothesize that as learning and task optimization is improved overnight (Kuriyama et al, 2004), there is a corresponding decreased need for conscious mapping of spatial relationships between finger movements and position (Seitz et al, 1990;Toni et al, 1998;Muller et al, 2002), the consequence of which is reduced post-sleep parietal involvement.…”

Section: Discussionmentioning

confidence: 99%

“…Demonstrations of overnight, sleep-dependent learning have now been reported across both sensory (Karni et al, 1994;Gais et al, 2000;Stickgold et al, 2000a,b;Fenn et al, 2003;Atienza et al, 2004;Gaab et al, 2004) and motor (Smith and MacNeill, 1994;Fischer et al, 2002;Walker et al, 2002Walker et al, , 2003aKorman et al, 2003;Huber et al, 2004;Robertson et al, 2004;Kuriyama et al, 2004) skill memory domains.…”

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Sleep-dependent motor memory plasticity in the human brain

et al. 2005

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Abstract-Growing evidence indicates a role for sleep in off-line memory processing, specifically in post-training consolidation. In humans, sleep has been shown to trigger overnight learning on a motor-sequence memory task, while equivalent waking periods produce no such improvement. But while the behavioral characteristics of sleep-dependent motor learning become increasingly well characterized, the underlying neural basis remains unknown. Here we present functional magnetic resonance imaging data demonstrating a change in the representation of a motor memory after a night of sleep. Subjects trained on a motor-skill memory and 12 hours later, after either sleep or wake, were retested during functional magnetic resonance imaging. Following sleep relative to wake, regions of increased activation were expressed in the right primary motor cortex, medial prefrontal lobe, hippocampus and left cerebellum; changes that can support faster motor output and more precise mapping of key-press movements. In contrast, signal decreases were identified in parietal cortices, the left insular cortex, temporal pole and fronto-polar region, reflecting a reduced need for conscious spatial monitoring and a decreased emotional task burden. This evidence of an overnight, systems- A large body of evidence, spanning a wide range of neuroscientific disciplines, now describes evidence of sleepdependent learning in both humans and animals , already complemented by cellular and molecular models of sleep-dependent plasticity (Graves et al., 2001;Tononi and Cirelli, 2001;Benington and Frank, 2003). In particular, sleep has been implicated in the ongoing process of consolidation, following initial memory acquisition.Within the procedural memory domain, sleep in humans has been shown to trigger significant overnight learning enhancements, whereby performance is selectively improved across sleeping intervals, while equivalent waking periods confer no such performance benefit (for reviews see Walker, in press). Demonstrations of overnight, sleep-dependent learning have now been reported across both sensory (Karni et al., 1994;Gais et al., 2000; Stickgold et al., 2000a,b;Fenn et al., 2003;Atienza et al., 2004;Gaab et al., 2004) Regarding motor-sequence learning, Walker et al. (2002, 2003a,b) have shown that a night of sleep can trigger significant improvements in both performance speed and accuracy on a finger-tapping task, while equivalent periods of time awake do not result in any such learning enhancements. Furthermore, these overnight learning gains correlated with the amount of stage two non-rapid eye movement (NREM) sleep, particularly late in the night (Walker et al., 2002). Adding to these findings, it also appears that there is no transfer of sleep-dependent procedural learning to either new motor sequences, or to performance of the same sequence using the opposite hand (Fischer et al., 2002;Korman et al., 2003), suggesting that the influence of sleep is highly specific. But while the behavioral characteristics of sleep-dependent motor...

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Section: Discussionmentioning

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Sleep-dependent motor memory plasticity in the human brain

et al. 2005

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“…The search for mechanisms underlying the cognitive role of sleep showed that slow oscillations typical of non-rapid eye movement (NREM) sleep are augmented after learning 17 , are proportional to the amount of learning in preschoolers 18 and can increase learning when experimentally boosted 19 . These findings close a causal loop that relates mnemonic gain to early-sleep neural synchronization.…”

Section: R E V I E Wmentioning

confidence: 99%

Neuroscience and education: prime time to build the bridge

et al. 2014

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“…When sleep is restricted, an enhanced SWA response follows in the next sleep period. Enhanced SWA has been associated with improved cognitive performance (Huber et al, 2004), but it is not clear whether a selective reduction of SWA is associated with decreased performance. Here we show a conditional, CNS knockout of the adenosine receptor, AdoA1R gene, selectively attenuates the enhanced SWA response to restricted sleep, but not sleep duration.…”

Section: Department Of Psychiatry Utswmentioning

confidence: 99%

Purines 2008 Meeting 29 June – 2 July 2008, Copenhagen, Denmark

2008

Purinergic Signalling

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Chemosensory transduction, allows the brain to sense and regulate the levels of blood gasses such as CO2 and important metabolites such as glucose. At least one class of CO2 chemosensory cell at the ventral surface of the medulla releases ATP as a key step in the detection of CO2. We have studied the mechanisms of CO2-dependent ATP release at the ventral medullary surface and have discovered a new principle of CO2 chemosensory transduction. ATP is released via the gating of connexin 26 (Cx26) hemichannels to mediate the adaptive ventilatory response to elevated CO2. The Cx26 channels are located only in the pia mater and sub-pial astrocytes. This very outermost layer of the brain, comprised of non-neuronal cells, thus has a key role in the detection of CO2. I will review our data and that of others suggesting a role for ATP-signalling in development, comparing and contrasting development of later structures such as the retina, and cortex with very early developmental events -genetic specification of the eye field itself. I will suggest that there are general principles of ATP signalling in these developmental contexts: namely release of ATP through gap junction hemichannels to evoke intracellular Ca2+ waves in neighbouring cells through activation of P2Y receptors. This suggests two important conclusions -that gap junction hemichannels may play a critical role in intercellular signalling in early development; and that their more general involvement in ATP-signalling can act as a unifying mechanistic principle across highly divergent physiological and developmental signalling contexts.Adenosine -an endogenous distress signal Adenosine is known to modulate the function of most organ systems of the body. It is formed from breakdown of intra-or extracellular adenine nucleotides -mostly in response to stressful situations such as low energy supply or cell damage. Adenosine therefore is an endogenous distress signal. Adenosine acts on four G protein coupled receptors -A 1 , A 2A , A 2B and A 3 . Adenosine is more potent at A 1 , A 2A , and A 3 than at A 2B receptors. The degree of stimulation by endogenous adenosine is determined, not only by the levels of extracellular adenosine, but also by the density of the receptors. Therefore even the low basal levels of adenosine that are always present in extracellular fluids may be sufficient to activate e.g. Purinergic Signalling (2008) 4 (Suppl 1):S1-S210 DOI 10.1007/s11302-008-9116-0 adenosine A 2A receptors where they are very abundant. It is known that A 2A receptors are particularly abundant on a subset of neurons in the basal ganglia that project i.a.-to globus pallidus. This tonic activation of A 2A receptors can be antagonized by the most widely used of all drugs-caffeine. The overview will briefly deal with roles of adenosine in several organ systems and from my own and other laboratories. I will also pay brief homage to a pioneer in the area -Dr John W. Daly who passed away earlier this year. Microglia listening to neurons through purinergic receptorsKazuhide Inoue...

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Local sleep and learning

Cited by 1,660 publications

References 28 publications

Sleep-dependent motor memory plasticity in the human brain

Sleep-dependent motor memory plasticity in the human brain

Neuroscience and education: prime time to build the bridge

Purines 2008 Meeting 29 June – 2 July 2008, Copenhagen, Denmark

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