Spinal TRPC3 promotes neuropathic pain and coordinates phospholipase C-induced mechanical hypersensitivity.

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Tác giả: Masashi Kakae, Shuji Kaneko, Yasuo Mori, Kazuki Nagayasu, Takayuki Nakagawa, Kyoko Sawada, Hisashi Shirakawa, Kosei Tamada, Shota Tobori, Nagi Uemura

Ngôn ngữ: eng

Ký hiệu phân loại: 949.59012 *Greece

Thông tin xuất bản: United States : Proceedings of the National Academy of Sciences of the United States of America , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 718020

Neuropathic pain is a debilitating chronic condition mainly caused by peripheral nerve injury. However, the cellular and molecular mechanisms underlying this condition remain unclear. Transient receptor potential canonical 3 (TRPC3), a TRP channel that is activated by downstream of the Gq-phospholipase C (PLC) axis, is expressed in the somatosensory system. Therefore, the present study investigated its pathophysiological role in neuropathic pain following peripheral nerve injury. Here, partial sciatic nerve ligation (pSNL) elicited mechanical and thermal hypersensitivity in wild-type mice, which was suppressed in TRPC3-KO mice. In situ hybridization revealed that TRPC3 is predominantly expressed in neurons in the spinal dorsal horn. Furthermore, spinal dorsal horn neuron-specific downregulation using miRNA attenuated pSNL-induced mechanical hypersensitivity. Spinal TRPC3 activation elicited acute mechanical hypersensitivity. Moreover, its genetic ablation reduced the mechanical hypersensitivity caused by spinal NK
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