Status: Bibliographieeintrag
Standort: ---
Exemplare:
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| Online-Ressource |
Verfasst von: | Cheng, Xing [VerfasserIn]  |
| Xiao, Fan [VerfasserIn]  |
| Xie, Rong [VerfasserIn]  |
| Hu, Haijun [VerfasserIn]  |
| Wan, Yong [VerfasserIn]  |
Titel: | Alternate thermal stimulation ameliorates thermal sensitivity and modulates calbindin-D 28K expression in lamina I and II and dorsal root ganglia in a mouse spinal cord contusion injury model |
Verf.angabe: | Xing Cheng, Fan Xiao, Rong Xie, Haijun Hu, Yong Wan |
E-Jahr: | 2021 |
Jahr: | February 2021 |
Umfang: | 16 S. |
Illustrationen: | Illustrationen |
Fussnoten: | Online veröffentlicht: 23 November 2020 ; Gesehen am 23.02.2024 |
Titel Quelle: | Enthalten in: Federation of American Societies for Experimental BiologyThe FASEB journal |
Ort Quelle: | Hoboken, NJ : Wiley, 1987 |
Band/Heft Quelle: | 35(2021), 2 vom: Feb., Artikel-ID e21173, Seite 1-16 |
ISSN Quelle: | 1530-6860 |
Abstract: | Neuropathic pain (NP) is a common complication that negatively affects the lives of patients with spinal cord injury (SCI). The disruption in the balance of excitatory and inhibitory neurons in the spinal cord dorsal horn contributes to the development of SCI and induces NP. The calcium-binding protein (CaBP) calbindin-D 28K (CaBP-28K) is highly expressed in excitatory interneurons, and the CaBP parvalbumin (PV) is present in inhibitory neurons in the dorsal horn. To better define the changes in the CaBPs contributing to the development of SCI-induced NP, we examined the changes in CaBP-28K and PV staining density in the lumbar (L4-6) lamina I and II, and their relationship with NP after mild spinal cord contusion injury in mice. We additionally examined the effects of alternate thermal stimulation (ATS). Compared with sham mice, injured animals developed mechanical allodynia in response to light mechanical stimuli and exhibited mechanical hyporesponsiveness to noxious mechanical stimuli. The decreased response latency to heat stimuli and increased response latency to cold stimuli at 7 days post injury suggested that the injured mice developed heat hyperalgesia and cold hypoalgesia, respectively. Temperature preference tests showed significant warm allodynia after injury. Animals that underwent ATS (15-18 and 35-40°C; +5 minutes/stimulation/day; 5 days/week) displayed significant amelioration of heat hyperalgesia, cold hypoalgesia, and warm allodynia after 2 weeks of ATS. In contrast, mechanical sensitivity was not influenced by ATS. Analysis of the CaBP-28K positive signal in L4-6 lamina I and II indicated an increase in staining density after SCI, which was associated with an increase in the number of CaBP-28K-stained L4-6 dorsal root ganglion (DRG) neurons. ATS decreased the CaBP-28K staining density in L4-6 spinal cord and DRG in injured animals, and was significantly and strongly correlated with ATS alleviation of pain behavior. The expression of PV showed no changes in lamina I and II after ATS in SCI animals. Thus, ATS partially decreases the pain behavior after SCI by modulating the changes in CaBP-associated excitatory-inhibitory neurons. |
DOI: | doi:10.1096/fj.202001775R |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext: https://doi.org/10.1096/fj.202001775R |
| Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1096/fj.202001775R |
| DOI: https://doi.org/10.1096/fj.202001775R |
Datenträger: | Online-Ressource |
Sprache: | eng |
Sach-SW: | alternate thermal stimulation |
| calbindin-D 28K |
| correlation |
| neuropathic pain |
| parvalbumin |
| spinal cord injury |
K10plus-PPN: | 1881507432 |
Verknüpfungen: | → Zeitschrift |
Alternate thermal stimulation ameliorates thermal sensitivity and modulates calbindin-D 28K expression in lamina I and II and dorsal root ganglia in a mouse spinal cord contusion injury model / Cheng, Xing [VerfasserIn]; February 2021 (Online-Ressource)
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