Increase in NREM sleep slow waves following injections of sodium oxybate in the mouse cerebral cortex and the role of somatostatin‐positive interneurons

Spano, Giovanna Maria; Cavelli, Matías; Marshall, William; Tononi, Giulio; Cirelli, Chiara

doi:10.1111/ejn.15846

Cited by 7 publications

(5 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent evidence shows that active inhibition generated by somatostatin-positive (SOM+) cells is directly related to the slow wave's onset (Funk et al, 2017). Furthermore, both the decrease in the firing of these cells and their chemogenetic inhibition decrease delta and increase sigma bands (Funk et al, 2017;Niethard et al, 2018;Spano et al, 2022). In that sense, our results suggest that the IS could represent a disinhibited state with a progressive withdrawal of SOM+ tone.…”

Section: Temporal Dynamics Of the Issupporting

confidence: 50%

Characterizing the power spectrum dynamics of the NREM to REM sleep transition

Serantes

Cavelli

González

et al. 2023

Preprint

View full text Add to dashboard Cite

The transition from NREM to REM sleep is considered a transitional or intermediate stage (IS), characterized by high amplitude spindles in the frontal cortex and theta activity in the occipital cortex. Early reports in rats showed an IS lasting from 1 to 5 s, but recent studies suggested a longer duration of this stage. To further characterize the IS, we analyzed its spectral characteristics on electrocorticogram (ECoG) recordings of the olfactory bulb (OB), motor (M1), somato-sensory (S1) and secondary visual cortex (V2) in twelve Wistar male adult rats. By comparing the IS to consolidated NREM/REM epochs, our results reveal that the IS has specific power spectral patterns that statistically differ from both NREM and REM sleep states. Specifically, the main findings were that sigma (11-16 Hz) and beta (17-30 Hz) power in OB, M1, and S1 increased during the IS compared to NREM and REM sleep and began 55 s before REM sleep onset. Additionally, low gamma (31-48 Hz) in the OB started transitioning from NREM levels to REM ones 65 s before its onset. Finally, the high-frequency oscillations (102-198 Hz) in OB, M1, and S1 showed a power increase that began 40 s before REM sleep and reached REM sleep values 10 s after its onset. Thus, we argue that the NREM to REM transition contains its own spectral profile and is more extended than previously described.

show abstract

Section: Temporal Dynamics Of the Issupporting

confidence: 50%

Characterizing the power spectrum dynamics of the NREM to REM sleep transition

Serantes

Cavelli

González

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Wake was identified by high muscle activity and low‐amplitude, high‐frequency EEG activity. NREM sleep was characterized by low muscle tone and high‐amplitude, low‐frequency EEG activity, while during REM sleep, low EMG activity with occasional twitches was associated with wake‐like, low‐amplitude, high‐frequency EEG activity and strong theta (5–9 Hz) activity in the parietal electrodes (Spano et al, 2022).…”

Section: Methodsmentioning

confidence: 99%

Effects of non‐rapid eye movement sleep on the cortical synaptic expression of GluA1‐containing AMPA receptors

Squarcio,

Tononi,

Cirelli

2024

Eur J of Neuroscience

Self Cite

View full text Add to dashboard Cite

Converging electrophysiological, molecular and ultrastructural evidence supports the hypothesis that sleep promotes a net decrease in excitatory synaptic strength, counteracting the net synaptic potentiation caused by ongoing learning during waking. However, several outstanding questions about sleep‐dependent synaptic weakening remain. Here, we address some of these questions by using two established molecular markers of synaptic strength, the levels of the AMPA (alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid) receptors containing the GluA1 subunit and the phosphorylation of GluA1 at serine 845 (p‐GluA1(845)). We previously found that, in the rat cortex and hippocampus, these markers are lower after 6–8 h of sleep than after the same time spent awake. Here, we measure GluA1 and p‐GluA1(845) levels in synaptosomes of mouse cortex after 5 h of either sleep, sleep deprivation, recovery sleep after sleep deprivation or selective REM sleep deprivation (32 C57BL/B6 adult mice, 16 females). We find that relative to after sleep deprivation, these synaptic markers are lower after sleep independent of whether the mice were allowed to enter REM sleep. Moreover, 5 h of recovery sleep following acute sleep deprivation is enough to renormalize their expression. Thus, the renormalization of GluA1 and p‐GluA1(845) expression crucially relies on NREM sleep and can occur in a few hours of sleep after acute sleep deprivation.

show abstract

“…Wake was identified by high muscle activity and low amplitude, high frequency EEG activity. NREM sleep was characterized by low muscle tone and high amplitude, low frequency EEG activity, while during REM sleep low EMG activity with occasional twitches was associated with wake-like, low amplitude, high frequency EEG activity and strong theta (5-9 Hz) activity in the parietal electrodes (Spano et al, 2022).…”

Section: Eeg Data Acquisition (Rem Sleep Deprivation)mentioning

confidence: 99%

Effects of NREM sleep on cortical synapses

Squarcio,

Tononi,

Cirelli

2024

Preprint

View full text Add to dashboard Cite

Converging electrophysiological, molecular, and ultrastructural evidence supports the hypothesis that sleep promotes a net decrease in excitatory synaptic strength, counteracting the net synaptic potentiation caused by ongoing learning during waking. However, several outstanding questions about sleep-dependent synaptic weakening remain. Here, we address some of these questions by using two established molecular markers of synaptic strength, the levels of the calcium-permeable AMPA (Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid) receptors containing the GluA1 subunit, and the phosphorylation of GluA1 at serine 845. We previously found that, in the rat cortex and hippocampus, these markers are lower after 6-8 hours of sleep than after the same time spent awake. Here, we measure GluA1 expression in mouse cortex after 5 hours of either sleep, sleep deprivation, recovery sleep after sleep deprivation, or selective REM sleep deprivation (32 C57BL/B6 adult mice, 16 females). We find that relative to after sleep deprivation, synaptic GluA1 expression is lower after sleep independent of whether the mice were allowed to enter REM sleep. Moreover, 5 hours of recovery sleep following acute sleep deprivation are enough to renormalize GluA1 expression. In a pilot study in old mice (12 C57BL/B6 male mice, 20-month-old) we also find that GluA1 expression is high after sleep deprivation and low after sleep and recovery sleep. Thus, the renormalization of GluA1 expression crucially relies on NREM sleep and can occur in a few hours of sleep after acute sleep deprivation. Moreover, as measured by GluA1 expression, it appears that sleep-dependent synaptic weakening is unaffected by aging.

show abstract

Increase in NREM sleep slow waves following injections of sodium oxybate in the mouse cerebral cortex and the role of somatostatin‐positive interneurons

Cited by 7 publications

References 57 publications

Characterizing the power spectrum dynamics of the NREM to REM sleep transition

Characterizing the power spectrum dynamics of the NREM to REM sleep transition

Effects of non‐rapid eye movement sleep on the cortical synaptic expression of GluA1‐containing AMPA receptors

Effects of NREM sleep on cortical synapses

Contact Info

Product

Resources

About