ArticleThe Journal of physiology2015
Sleep spindles and human cortical nociception: a surface and intracerebral electrophysiological study.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- The pain alarm response - an example of how conscious awareness shapes pain perception.Scientific reports · 2019Trial
- Subjective sleep quality predict clinical pain severity more strongly than polysomnographic parameters: Machine learning findings from a cross-sectional study.Sleep medicine · 2026Article
- Filtering the noise: a cerebellar-centered framework for understanding and treating mental illness -a paradigm shift in psychiatry.Frontiers in psychiatry · 2026Article
- Calcitonin Gene-Related Peptide (CGRP)-Expressing Neurons in the External Lateral Parabrachial Area Regulate Pain-Induced Sleep Disturbances.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identifying the Brain Circuits that Regulate Pain-Induced Sleep Disturbances.bioRxiv : the preprint server for biology · 2024Article
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- Intracortical Functional Connectivity Predicts Arousal to Noxious Stimuli during Sleep in Humans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- A mechanism for learning with sleep spindles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Review
- Absent sleep EEG spindle activity in GluA1 (Gria1) knockout mice: relevance to neuropsychiatric disorders.Translational psychiatry · 2018Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
key pointsSleep spindle are usually considered to play a major role in inhibiting sensory inputs. Using nociceptive stimuli in humans, we tested the effect of spindles on behavioural, autonomic and cortical responses in two experiments using surface and intracerebral electroencephalographic recordings. We found that sleep spindles do not prevent arousal reactions to nociceptive stimuli and that autonomic reactivity to nociceptive inputs is not modulated by spindle activity. Moreover, neither the surface sensory, nor the insular evoked responses were modulated by the spindle, as detected at the surface or within the thalamus. The present study comprises the first investigation of the effect of spindles on nociceptive information processing and the results obtained challenge the classical inhibitory effect of spindles. ABSTRACT: Responsiveness to environmental stimuli declines during sleep, and sleep spindles are often considered to play a major role in inhibiting sensory inputs. In the present study, we tested the effect of spindles on behavioural, autonomic and cortical responses to pain, in two experiments assessing surface and intracerebral responses to thermo-nociceptive laser stimuli during the all-night N2 sleep stage. The percentage of arousals remained unchanged as a result of the presence of spindles. Neither cortical nociceptive responses, nor autonomic cardiovascular reactivity were depressed when elicited within a spindle. These results could be replicated in human intracerebral recordings, where sleep spindle activity in the posterior thalamus failed to depress the thalamocortical nociceptive transmission, as measured by sensory responses within the posterior insula. Hence, the assumed inhibitory effect of spindles on sensory inputs may not apply to the nociceptive system, possibly as a result of the specificity of spinothalamic pathways and the crucial role of nociceptive information for homeostasis. Intriguingly, a late scalp response commonly considered to reflect high-order stimulus processing (the 'P3' potential) was significantly enhanced during spindling, suggesting a possible spindle-driven facilitation, rather than attenuation, of cortical nociception.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.