Publisher Correction: Cortical dendritic activity correlates with spindle-rich oscillations during sleep in rodents

Seibt, Julie; Richard, Clément J.; Sigl‐Glöckner, Johanna; Kaplan, D.; Doron, Guy; Limoges, Denis de; Bocklisch, Christina; Larkum, Matthew E.

doi:10.1038/s41467-017-01652-8

Cited by 10 publications

(6 citation statements)

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“…Two recent findings suggest potential underlying mechanisms. An in vivo imaging study by Seibt et al recently described high levels of dendritic calcium influx (which occurred in a synchronized manner among neighboring cortical neurons) which was tightly linked to spindle frequency EEG activity [72]. Insofar as increasing dendritic calcium is a consistent correlate of (and indeed prerequisite for) LTP [73], this finding is completely consistent with other results linking spindle-frequency activity to synaptic potentiation in thalamocortical circuits.…”

Section: Messa DI Voce: Thalamocortical Sleep Spindlessupporting

confidence: 75%

“…Insofar as increasing dendritic calcium is a consistent correlate of (and indeed prerequisite for) LTP [73], this finding is completely consistent with other results linking spindle-frequency activity to synaptic potentiation in thalamocortical circuits. Critically, this increase in dendritic calcium was not associated with a concomitant increase in neuronal spiking during spindle-rich sleep [72]-suggesting a non-Hebbian form of EPSP-driven plasticity, dependent on intra-EPSP timing [74,75] during spindling. An explanation of the unique conditions found during spindles in the Seibt et al study (i.e.…”

Section: Messa DI Voce: Thalamocortical Sleep Spindlesmentioning

confidence: 85%

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How rhythms of the sleeping brain tune memory and synaptic plasticity

Puentes-Mestril

Roach

Niethard

et al. 2019

Sleep

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Decades of neurobehavioral research has linked sleep-associated rhythms in various brain areas to improvements in cognitive performance. However, it remains unclear what synaptic changes might underlie sleep-dependent declarative memory consolidation and procedural task improvement, and why these same changes appear not to occur across a similar interval of wake. Here we describe recent research on how one specific feature of sleep—network rhythms characteristic of rapid eye movement and non-rapid eye movement—could drive synaptic strengthening or weakening in specific brain circuits. We provide an overview of how these rhythms could affect synaptic plasticity individually and in concert. We also present an overarching hypothesis for how all network rhythms occurring across the sleeping brain could aid in encoding new information in neural circuits.

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Section: Messa DI Voce: Thalamocortical Sleep Spindlessupporting

confidence: 75%

Section: Messa DI Voce: Thalamocortical Sleep Spindlesmentioning

confidence: 85%

How rhythms of the sleeping brain tune memory and synaptic plasticity

Puentes-Mestril

Roach

Niethard

et al. 2019

Sleep

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“…Through these cross-frequency interactions SSs could augment/prolong calcium conductance and trigger the signaling cascades required for consolidative plasticity. Seibt et al ( 2017 ) demonstrate that SS associated sigma activity elevates dendritic calcium, providing experimental evidence that systems memory consolidation associated oscillations can evoke changes in dendritic calcium kinetics/dynamics. In sum, interaction amongst dynamical brain rhythms orchestrates membrane properties to gate the synaptic plasticity necessary for consolidative mnemonic processing during sleep.…”

Section: Nrems Oscillations and Memory Consolidationmentioning

confidence: 98%

“…The relatively high oscillatory frequency of SSs makes these rhythms unlikely to trigger depressive STDP mechanisms. However, given that SSs have been demonstrated to elicit calcium transients in dendrites (Seibt et al, 2017 ) it is possible that particular SS waveforms, or SSs timed to occur in isolation from SPW-R or SO depolarizations, could cause the activation of depressive biochemical cascades.…”

Section: Nrems Oscillations and Forgettingmentioning

confidence: 99%

Remembering to Forget: A Dual Role for Sleep Oscillations in Memory Consolidation and Forgetting

Langille

2019

Front. Cell. Neurosci.

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It has been known since the time of patient H. M. and Karl Lashley’s equipotentiality studies that the hippocampus and cortex serve mnestic functions. Current memory models maintain that these two brain structures accomplish unique, but interactive, memory functions. Specifically, most modeling suggests that memories are rapidly acquired during waking experience by the hippocampus, before being later consolidated into the cortex for long-term storage. Sleep has been shown to be critical for the transfer and consolidation of memories in the cortex. Like memory consolidation, a role for sleep in adaptive forgetting has both historical precedent, as Francis Crick suggested in 1983 that sleep was for “reverse-learning,” and recent empirical support. In this article I review the evidence indicating that the same brain activity involved in sleep replay associated memory consolidation is responsible for sleep-dependent forgetting. In reviewing the literature, it became clear that both a cellular mechanism for systems consolidation and an agreed upon general, as well as cellular, mechanism for sleep-dependent forgetting is seldom discussed or is lacking. I advocate here for a candidate cellular systems consolidation mechanism wherein changes in calcium kinetics and the activation of consolidative signaling cascades arise from the triple phase locking of non-rapid eye movement sleep (NREMS) slow oscillation, sleep spindle and sharp-wave ripple rhythms. I go on to speculatively consider several sleep stage specific forgetting mechanisms and conclude by discussing a notional function of NREM-rapid eye movement sleep (REMS) cycling. The discussed model argues that the cyclical organization of sleep functions to first lay down and edit and then stabilize and integrate engrams. All things considered, it is increasingly clear that hallmark sleep stage rhythms, including several NREMS oscillations and the REMS hippocampal theta rhythm, serve the dual function of enabling simultaneous memory consolidation and adaptive forgetting. Specifically, the same sleep rhythms that consolidate new memories, in the cortex and hippocampus, simultaneously organize the adaptive forgetting of older memories in these brain regions.

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“…On the other hand, recent calcium imaging studies of the mouse neocortex have demonstrated higher activity of Sst+ interneurons in superficial cortical layers during wake versus NREM sleep (64,65). This effect (which would lead to reductions in dendritetargeted inhibition during sleep) may be related to the recent finding of dendritic calcium spikes in these cortical layers during NREM oscillations (66). Critically, the activation of neocortical Sst+ interneurons during active wakefulness is driven by cholinergic signaling (67).…”

Section: Neurosciencementioning

confidence: 99%

Sleep loss drives acetylcholine- and somatostatin interneuron–mediated gating of hippocampal activity to inhibit memory consolidation

Delorme

Wang

Kuhn

et al. 2021

Proc. Natl. Acad. Sci. U.S.A.

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Sleep loss disrupts consolidation of hippocampus-dependent memory. To characterize effects of learning and sleep loss, we quantified activity-dependent phosphorylation of ribosomal protein S6 (pS6) across the dorsal hippocampus of mice. We find that pS6 is enhanced in dentate gyrus (DG) following single-trial contextual fear conditioning (CFC) but is reduced throughout the hippocampus after brief sleep deprivation (SD; which disrupts contextual fear memory [CFM] consolidation). To characterize neuronal populations affected by SD, we used translating ribosome affinity purification sequencing to identify cell type–specific transcripts on pS6 ribosomes (pS6-TRAP). Cell type–specific enrichment analysis revealed that SD selectively activated hippocampal somatostatin-expressing (Sst+) interneurons and cholinergic and orexinergic hippocampal inputs. To understand the functional consequences of SD-elevated Sst+ interneuron activity, we used pharmacogenetics to activate or inhibit hippocampal Sst+ interneurons or cholinergic input from the medial septum. The activation of either cell population was sufficient to disrupt sleep-dependent CFM consolidation by gating activity in granule cells. The inhibition of either cell population during sleep promoted CFM consolidation and increased S6 phosphorylation among DG granule cells, suggesting their disinhibition by these manipulations. The inhibition of either population across post-CFC SD was insufficient to fully rescue CFM deficits, suggesting that additional features of sleeping brain activity are required for consolidation. Together, our data suggest that state-dependent gating of DG activity may be mediated by cholinergic input and local Sst+ interneurons. This mechanism could act as a sleep loss–driven inhibitory gate on hippocampal information processing.

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Publisher Correction: Cortical dendritic activity correlates with spindle-rich oscillations during sleep in rodents

Cited by 10 publications

References 0 publications

How rhythms of the sleeping brain tune memory and synaptic plasticity

How rhythms of the sleeping brain tune memory and synaptic plasticity

Remembering to Forget: A Dual Role for Sleep Oscillations in Memory Consolidation and Forgetting

Sleep loss drives acetylcholine- and somatostatin interneuron–mediated gating of hippocampal activity to inhibit memory consolidation

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