9 28

Cited 0 times in

Inhibiting Nav1.7 channels in pulpitis: An in vivo study on neuronal hyperexcitability

Authors
 Kyung Hee Lee  ;  Un Jeng Kim  ;  Myeounghoon Cha  ;  Bae Hwan Lee 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.717 : 150044, 2024-07 
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN
 0006-291X 
Issue Date
2024-07
MeSH
Animals ; Disease Models, Animal ; Intercellular Signaling Peptides and Proteins ; Male ; Mice ; NAV1.7 Voltage-Gated Sodium Channel* / genetics ; NAV1.7 Voltage-Gated Sodium Channel* / metabolism ; Nerve Tissue Proteins / metabolism ; Neurons / metabolism ; Proto-Oncogene Proteins c-fos / metabolism ; Pulpitis* / metabolism ; Pulpitis* / pathology ; Trigeminal Ganglion / metabolism ; Voltage-Gated Sodium Channel Blockers / pharmacology
Keywords
In vivo ; ProTx-II ; Pulpitis ; Trigeminal ganglion (TG) ; Voltage-gated sodium channel 1.7 (Nav1.7)
Abstract
Pulpitis constitutes a significant challenge in clinical management due to its impact on peripheral nerve tissue and the persistence of chronic pain. Despite its clinical importance, the correlation between neuronal activity and the expression of voltage-gated sodium channel 1.7 (Nav1.7) in the trigeminal ganglion (TG) during pulpitis is less investigated. The aim of this study was to examine the relationship between experimentally induced pulpitis and Nav1.7 expression in the TG and to investigate the potential of selective Nav1.7 modulation to attenuate TG abnormal activity associated with pulpitis. Acute pulpitis was induced at the maxillary molar (M1) using allyl isothiocyanate (AITC). The mice were divided into three groups: control, pulpitis model, and pulpitis model treated with ProTx-II, a selective Nav1.7 channel inhibitor. After three days following the surgery, we conducted a recording and comparative analysis of the neural activity of the TG utilizing in vivo optical imaging. Then immunohistochemistry and Western blot were performed to assess changes in the expression levels of extracellular signal-regulated kinase (ERK), c-Fos, collapsin response mediator protein-2 (CRMP2), and Nav1.7 channels. The optical imaging result showed significant neurological excitation in pulpitis TGs. Nav1.7 expressions exhibited upregulation, accompanied by signaling molecular changes suggestive of inflammation and neuroplasticity. In addition, inhibition of Nav1.7 led to reduced neural activity and subsequent decreases in ERK, c-Fos, and CRMP2 levels. These findings suggest the potential for targeting overexpressed Nav1.7 channels to alleviate pain associated with pulpitis, providing practical pain management strategies.
Files in This Item:
T202403228.pdf Download
DOI
10.1016/j.bbrc.2024.150044
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Un Jeng(김은정) ORCID logo https://orcid.org/0000-0003-0968-0252
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
Cha, Myeoung Hoon(차명훈) ORCID logo https://orcid.org/0000-0002-7993-672X
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/199717
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse

Links