Journal of Shanghai Jiao Tong University (Medical Science) >

2025 , Vol. 45 >Issue 11: 1458 - 1465

DOI: https://doi.org/10.3969/j.issn.1674-8115.2025.11.005

Basic research

N-glycosylation of Cav3.2 channel in DRG neurons of myelinated A-fiber contributes to diabetic mechanical allodynia

  • LIAO Chenlong ,
  • LI Shuo ,
  • XU Xin ,
  • ZHANG Yue ,
  • ZHANG Wenchuan
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  • Department of Neurosurgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
ZHANG Wenchuan, E-mail: zhangwench88@sjtu.edu.cn.

Received date: 2025-06-02

  Accepted date: 2025-07-17

  Online published: 2025-12-03

Supported by

National Natural Science Foundation of China(81801219);Medical Innovation Research Project of Science and Technology Commission of Shanghai Municipality(21Y11906300);Natural Science Foundation of Shanghai(21ZR1438100)

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Abstract

Objective ·To investigate the association of Cav3.2 channel N-glycosylation in myelinated A-fiber dorsal root ganglion (DRG) neurons with diabetic mechanical allodynia (MA). Methods ·Diabetic rat models were induced by a single intraperitoneal injection of streptozotocin. Pain behavior assessments, including evaluations of MA and thermal hyperalgesia (TH), were conducted on a weekly basis. Diabetic rats exhibiting TH were subsequently categorized into two subcategories based on the onset of mechanical allodynia by the third week. The impact of N-glycosylation on both the expression of Cav3.2 channels in DRG neurons and pain behaviors was investigated through sequential administration of neuraminidase (NEU) and TTA-P2, a selective blocker of T-type calcium channels, after C-unmyelinated fiber blockage by the application of resiniferatoxin (RTX). The extent of Cav3.2 N-glycosylation was quantitatively compared between diabetic rats with and without MA by analyzing the N-terminal fragment of Cav3.2 following de-glycosylation. Results ·Higher levels of Cav3.2 expression in myelinated A-fiber DRG neurons were observed in diabetic rats with MA compared to those without MA (P<0.001). NEU-induced de-glycosylation led to a reduction in Cav3.2 expression across all groups, with diabetic rats with MA maintaining higher levels of the Cav3.2 expression than those without MA (P<0.05). It was observed that RTX eliminated only TH and not MA, whereas NEU had a restorative effect on both TH and MA, similar to TTA-P2. Diabetic rats with MA exhibited increased expression of N-terminal fragments compared to those without MA (P<0.001). Conclusion ·N-glycosylation of the Cav3.2 channel within DRG neurons of myelinated A-fiber is a contributing factor to diabetic MA.

Key words： diabetic peripheral neuropathy; Cav3.2 channel; mechanical allodynia; dorsal root ganglion; glycosylation

Cite this article

LIAO Chenlong , LI Shuo , XU Xin , ZHANG Yue , ZHANG Wenchuan . N-glycosylation of Cav3.2 channel in DRG neurons of myelinated A-fiber contributes to diabetic mechanical allodynia[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2025 , 45(11) : 1458 -1465 . DOI: 10.3969/j.issn.1674-8115.2025.11.005

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