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Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons
BACKGROUND: In the central nervous system, post-inhibitory rebound firing (RF) may mediate overactivity of neurons under pathophysiological condition. RF is also observed in dorsal root ganglion (IRA) neurons. However, the functional significance of RF in primary sensory neurons has remained unknown...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9342929/ https://www.ncbi.nlm.nih.gov/pubmed/35923842 http://dx.doi.org/10.2147/JPR.S370335 |
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author | Zhu, Tong Wei, Siqi Wang, Yuying |
author_facet | Zhu, Tong Wei, Siqi Wang, Yuying |
author_sort | Zhu, Tong |
collection | PubMed |
description | BACKGROUND: In the central nervous system, post-inhibitory rebound firing (RF) may mediate overactivity of neurons under pathophysiological condition. RF is also observed in dorsal root ganglion (IRA) neurons. However, the functional significance of RF in primary sensory neurons has remained unknown. After peripheral sensory nerve/neuron injury, DRG neurons exhibit hyperexcitability. Therefore, RF may play a role in neuropathic pain. METHODS: Chronic compression of DRG (CCD) is used as a neuropathic pain model. Rats were divided into 2 groups: Sham and CCD groups. Patch clamp was performed on the whole DRG and cultured DRG neurons to record RF and T-type Ca(2+) currents. The blocker of T-type Ca(2+) channels, NiCl(2), was applied to DRG neurons. RESULTS: Rebound neurons were more excitable than non-rebound neurons. And they discharged RF with prominent after depolarizing potentials, which were blocked by NiCl(2). After DRG injury, the proportion of rebound neurons augmented, and rebound neurons’ excitability increased. Meanwhile, the steady-state activation curve of T-type Ca(2+) channels was shifted toward the left. CONCLUSION: RF may be related to highly excitable neurons and sensitive to both depolarization and hyperpolarization. T-type Ca(2+) channels were critical to RF, potentially enhancing the spontaneous firing of rebound neurons in response to resting membrane potential fluctuations. |
format | Online Article Text |
id | pubmed-9342929 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-93429292022-08-02 Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons Zhu, Tong Wei, Siqi Wang, Yuying J Pain Res Original Research BACKGROUND: In the central nervous system, post-inhibitory rebound firing (RF) may mediate overactivity of neurons under pathophysiological condition. RF is also observed in dorsal root ganglion (IRA) neurons. However, the functional significance of RF in primary sensory neurons has remained unknown. After peripheral sensory nerve/neuron injury, DRG neurons exhibit hyperexcitability. Therefore, RF may play a role in neuropathic pain. METHODS: Chronic compression of DRG (CCD) is used as a neuropathic pain model. Rats were divided into 2 groups: Sham and CCD groups. Patch clamp was performed on the whole DRG and cultured DRG neurons to record RF and T-type Ca(2+) currents. The blocker of T-type Ca(2+) channels, NiCl(2), was applied to DRG neurons. RESULTS: Rebound neurons were more excitable than non-rebound neurons. And they discharged RF with prominent after depolarizing potentials, which were blocked by NiCl(2). After DRG injury, the proportion of rebound neurons augmented, and rebound neurons’ excitability increased. Meanwhile, the steady-state activation curve of T-type Ca(2+) channels was shifted toward the left. CONCLUSION: RF may be related to highly excitable neurons and sensitive to both depolarization and hyperpolarization. T-type Ca(2+) channels were critical to RF, potentially enhancing the spontaneous firing of rebound neurons in response to resting membrane potential fluctuations. Dove 2022-07-26 /pmc/articles/PMC9342929/ /pubmed/35923842 http://dx.doi.org/10.2147/JPR.S370335 Text en © 2022 Zhu et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhu, Tong Wei, Siqi Wang, Yuying Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title | Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title_full | Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title_fullStr | Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title_full_unstemmed | Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title_short | Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons |
title_sort | post-inhibitory rebound firing of dorsal root ganglia neurons |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9342929/ https://www.ncbi.nlm.nih.gov/pubmed/35923842 http://dx.doi.org/10.2147/JPR.S370335 |
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