Increased Expression of TRPV1 in the Central Nucleus of the Amygdala Is Involved in Orthodontic Pain in Rats
Transient receptor potential vanilloid type 1 (TRPV1) is known to gate nociceptive signals, while the central amygdala (CeA) plays a key role in encoding pain and avoidance behaviors; however, whether TRPV1 within CeA mediate orthodontic tooth-moving pain remains unclear. To investigate this, we examined the role of TRPV1 in the CeA using a rat model of experimental tooth movement. A total of 118 Sprague-Dawley rats were divided into control, 30 g, 50 g, and 80 g force groups. Micro-CT confirmed successful tooth movement, and the 50 g force was selected as optimal. Pain was assessed by mechanical hypersensitivity using the von Frey test, face-grooming, and the Rat Grimace Scale (RGS). All measures showed maximal changes at day 1 and returned to baseline by day 7. Immunohistochemistry and western blot analysis in the 50 g group revealed upregulation of TRPV1 in the CeA following force application, a trajectory that paralleled the pain behavioral responses. These findings indicate that experimental tooth movement upregulates TRPV1 in the CeA and that this channel contributes to orthodontic pain.
Authors
- Shuang Wang (ORCID: https://orcid.org/0000-0001-5037-4316)
- Hu Qiao (ORCID: https://orcid.org/0000-0003-2323-4881)
- Xiaoyu Tang (ORCID: https://orcid.org/0009-0000-7373-7618)
- Zhiping Hu (ORCID: https://orcid.org/0000-0001-5672-9683)
- Yu‐Mian Shu (ORCID: https://orcid.org/0000-0003-0804-4430)
- Ning Wang (ORCID: https://orcid.org/0000-0003-1745-1425)
- Rui Wang
- Jiayi Zhou (ORCID: https://orcid.org/0000-0001-8865-3070)
- Young Ae Kang (ORCID: https://orcid.org/0000-0002-6543-6521)
- Yuhuan Jiang (ORCID: https://orcid.org/0009-0008-2025-9999)
Institutions
- Xi'an Jiaotong University (CN)
Publication Details
- Journal
- International Journal of Molecular Sciences
- Published
- 2025-11-22
- DOI
- https://doi.org/10.3390/ijms262311296
- Primary Topic
- Pain Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00