Role of TRPV1 in electroacupuncture‐mediated signal to the primary sensory cortex during regulation of the swallowing function

Author:

Yuan Si12ORCID,Qiu Bo1,Liang Ying1,Deng Bing1,Xu Jing1,Tang Xiaorong1ORCID,Wu Junshang1,Zhou Sheng1,Li Zeli1,Li Hongzhu3,Ye Qiuping14ORCID,Wang Lin1,Cui Shuai5,Tang Chunzhi1,Yi Wei1,Yao Lulu1,Xu Nenggui1ORCID

Affiliation:

1. South China Research Center for Acupuncture and Moxibustion, Medical College of Acu‐Moxi and Rehabilitation Guangzhou University of Chinese Medicine Guangzhou China

2. Department of Rehabilitation of Traditional Chinese Medicine Hunan University of Chinese Medicine Changsha China

3. Rehabilitation Center First Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou China

4. Department of Rehabilitation Medicine, The Third Affiliated Hospital Sun Yat‐sen University Guangzhou China

5. Research Institute of Acupuncture and Meridian, College of Acupuncture and Moxibustion Anhui University of Chinese Medicine Hefei China

Abstract

AbstractAimsElectroacupuncture (EA) at the Lianquan (CV23) could alleviate swallowing dysfunction. However, current knowledge of its neural modulation focused on the brain, with little evidence from the periphery. Transient receptor potential channel vanilloid subfamily 1 (TRPV1) is an ion channel predominantly expressed in sensory neurons, and acupuncture can trigger calcium ion (Ca2+) wave propagation through active TRPV1 to deliver signals. The present study aimed to investigate whether TRPV1 mediated the signal of EA to the primary sensory cortex (S1) during regulation of swallowing function.MethodsBlood perfusion was evaluated by laser speckle contrast imaging (LSCI), and neuronal activity was evaluated by fiber calcium recording and c‐Fos staining. The expression of TRPV1 was detected by RNA‐seq analysis, immunofluorescence, and ELISA. In addition, the swallowing function was assessed by in vivo EMG recording and water consumption test.ResultsEA treatment potentiated blood perfusion and neuronal activity in the S1, and this potentiation was absent after injecting lidocaine near CV23. TRPV1 near CV23 was upregulated by EA‐CV23. The blood perfusion at CV23 was decreased in the TRPV1 hypofunction mice, while the blood perfusion and the neuronal activity of the S1 showed no obvious change. These findings were also present in post‐stroke dysphagia (PSD) mice.ConclusionThe TRPV1 at CV23 after EA treatment might play a key role in mediating local blood perfusion but was not involved in transferring EA signals to the central nervous system (CNS). These findings collectively suggested that TRPV1 may be one of the important regulators involved in the mechanism of EA treatment for improving swallowing function in PSD.

Publisher

Wiley

Subject

Pharmacology (medical),Physiology (medical),Psychiatry and Mental health,Pharmacology

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