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9. TRPC3/6 Channels Mediate Mechanical Pain Hypersensitivity via Enhancement of Nociceptor Excitability and of Spinal Synaptic Transmission

Author

Zhi‐Chuan Sun, Wen‐Juan Han, Zhi‐Wei Dou, Na Lu, Xu Wang, Fu‐Dong Wang, Sui‐Bin Ma, Zhi‐Cheng Tian, Hang Xian, Wan‐Neng Liu, Ying‐Ying Liu, Wen‐Bin Wu, Wen‐Guang Chu, Huan Guo, Fei Wang, Hui Ding, Yuan‐Ying Liu, Hui‐Ren Tao, Marc Freichel, Lutz Birnbaumer, Zhen‐Zhen Li, Rou‐Gang Xie, Sheng‐Xi Wu, and Ceng Luo

Subjects
mechanical pain hypersensitivity, nociceptor, synaptic potentiation, TRPC3, TRPC6, Science
Abstract

Abstract Patients with tissue inflammation or injury often experience aberrant mechanical pain hypersensitivity, one of leading symptoms in clinic. Despite this, the molecular mechanisms underlying mechanical distortion are poorly understood. Canonical transient receptor potential (TRPC) channels confer sensitivity to mechanical stimulation. TRPC3 and TRPC6 proteins, coassembling as heterotetrameric channels, are highly expressed in sensory neurons. However, how these channels mediate mechanical pain hypersensitivity has remained elusive. It is shown that in mice and human, TRPC3 and TRPC6 are upregulated in DRG and spinal dorsal horn under pathological states. Double knockout of TRPC3/6 blunts mechanical pain hypersensitivity, largely by decreasing nociceptor hyperexcitability and spinal synaptic potentiation via presynaptic mechanism. In corroboration with this, nociceptor‐specific ablation of TRPC3/6 produces comparable pain relief. Mechanistic analysis reveals that upon peripheral inflammation, TRPC3/6 in primary sensory neurons get recruited via released bradykinin acting on B1/B2 receptors, facilitating BDNF secretion from spinal nociceptor terminals, which in turn potentiates synaptic transmission through TRPC3/6 and eventually results in mechanical pain hypersensitivity. Antagonizing TRPC3/6 in DRG relieves mechanical pain hypersensitivity in mice and nociceptor hyperexcitability in human. Thus, TRPC3/6 in nociceptors is crucially involved in pain plasticity and constitutes a promising therapeutic target against mechanical pain hypersensitivity with minor side effects.

Published
2024
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36. Mechanical force-induced interlayer sliding in interfacial ferroelectrics.

Author

Guan, Zhao, Wei, Lu-qi, Fan, Wen-cheng, Sun, Yi-chen, Cao, Wei, Tian, Ming, Wan, Neng, Tong, Wen-yi, Chen, Bin-bin, Xiang, Ping-hua, Duan, Chun-gang, and Zhong, Ni

Subjects
FERROELECTRICITY, FERROELECTRIC crystals, TRIANGLES, SUPERLATTICES
Abstract

Moiré superlattices in two-dimensional stacks have attracted worldwide interest due to their unique electronic properties. A typical example is the moiré ferroelectricity, where adjacent moirés exhibit opposite spontaneous polarization that can be switched through interlayer sliding. However, in contrast to ideal regular ferroelectric moiré domains (equilateral triangles) built in most theoretical models, the unavoidable irregular moiré supercells (non-equilateral triangles) induced by external strain fields during the transfer process have been given less attention. Manipulation of controllable polarization evolutions is also a big challenge due to an interlinked network of polarized domains. In this study, we employ a sliding-disturb measurement to examine and modulate these irregular moirés via mechanical force. By introducing a curved substrate, the irregular moirés are fabricated, and three distinct types of moiré domains with different patterns are identified and modulated by external mechanical force disturbing. They exhibit reduced pinning forces when the shear direction is not aligned with the strain direction. The shift of the moirés is observed to be orthogonal to the shear direction. This work offers an effective pathway for the controlled switch of the polarization in interfacial ferroelectricity. Manipulation of controllable polarization evolutions is a big challenge. The authors fabricate the irregular moirés, identifying three distinct types of moiré domains with different patterns, modulating them by external mechanical force disturbing. [ABSTRACT FROM AUTHOR]

Published
2025
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