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Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition
It is known that the thalamocortical loop plays a crucial role in the encoding of sensory–discriminative features of painful stimuli. However, only a few studies have addressed the changes in thalamocortical dynamics that may occur after the onset of chronic pain. Our goal was to evaluate how the in...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Research Foundation
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188809/ https://www.ncbi.nlm.nih.gov/pubmed/22007162 http://dx.doi.org/10.3389/fnint.2011.00043 |
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author | Cardoso-Cruz, Helder Sameshima, Koichi Lima, Deolinda Galhardo, Vasco |
author_facet | Cardoso-Cruz, Helder Sameshima, Koichi Lima, Deolinda Galhardo, Vasco |
author_sort | Cardoso-Cruz, Helder |
collection | PubMed |
description | It is known that the thalamocortical loop plays a crucial role in the encoding of sensory–discriminative features of painful stimuli. However, only a few studies have addressed the changes in thalamocortical dynamics that may occur after the onset of chronic pain. Our goal was to evaluate how the induction of chronic neuropathic pain affected the flow of information within the thalamocortical loop throughout the brain states of the sleep–wake cycle. To address this issue we recorded local field potentials (LFPs) – both before and after the establishment of neuropathic pain in awake freely moving adult rats chronically implanted with arrays of multielectrodes in the lateral thalamus and primary somatosensory cortex. Our results show that the neuropathic injury induced changes in the number of wake and slow-wave-sleep (SWS) state episodes, and especially in the total number of transitions between brain states. Moreover, partial directed coherence – analysis revealed that the amount of information flow between cortex and thalamus in neuropathic animals decreased significantly, indicating that the overall thalamic activity had less weight over the cortical activity. However, thalamocortical LFPs displayed higher phase-locking during awake and SWS episodes after the nerve lesion, suggesting faster transmission of relevant information along the thalamocortical loop. The observed changes are in agreement with the hypothesis of thalamic dysfunction after the onset of chronic pain, and may result from diminished inhibitory effect of the primary somatosensory cortex over the lateral thalamus. |
format | Online Article Text |
id | pubmed-3188809 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Frontiers Research Foundation |
record_format | MEDLINE/PubMed |
spelling | pubmed-31888092011-10-17 Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition Cardoso-Cruz, Helder Sameshima, Koichi Lima, Deolinda Galhardo, Vasco Front Integr Neurosci Neuroscience It is known that the thalamocortical loop plays a crucial role in the encoding of sensory–discriminative features of painful stimuli. However, only a few studies have addressed the changes in thalamocortical dynamics that may occur after the onset of chronic pain. Our goal was to evaluate how the induction of chronic neuropathic pain affected the flow of information within the thalamocortical loop throughout the brain states of the sleep–wake cycle. To address this issue we recorded local field potentials (LFPs) – both before and after the establishment of neuropathic pain in awake freely moving adult rats chronically implanted with arrays of multielectrodes in the lateral thalamus and primary somatosensory cortex. Our results show that the neuropathic injury induced changes in the number of wake and slow-wave-sleep (SWS) state episodes, and especially in the total number of transitions between brain states. Moreover, partial directed coherence – analysis revealed that the amount of information flow between cortex and thalamus in neuropathic animals decreased significantly, indicating that the overall thalamic activity had less weight over the cortical activity. However, thalamocortical LFPs displayed higher phase-locking during awake and SWS episodes after the nerve lesion, suggesting faster transmission of relevant information along the thalamocortical loop. The observed changes are in agreement with the hypothesis of thalamic dysfunction after the onset of chronic pain, and may result from diminished inhibitory effect of the primary somatosensory cortex over the lateral thalamus. Frontiers Research Foundation 2011-08-23 /pmc/articles/PMC3188809/ /pubmed/22007162 http://dx.doi.org/10.3389/fnint.2011.00043 Text en Copyright © 2011 Cardoso-Cruz, Sameshima, Lima and Galhardo. http://www.frontiersin.org/licenseagreement This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with. |
spellingShingle | Neuroscience Cardoso-Cruz, Helder Sameshima, Koichi Lima, Deolinda Galhardo, Vasco Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title | Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title_full | Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title_fullStr | Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title_full_unstemmed | Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title_short | Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition |
title_sort | dynamics of circadian thalamocortical flow of information during a peripheral neuropathic pain condition |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188809/ https://www.ncbi.nlm.nih.gov/pubmed/22007162 http://dx.doi.org/10.3389/fnint.2011.00043 |
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