| Autor: |
Feng XJ; 1 Center for Experimental Medicine, the First Affiliated Hospital of Nanchang University, Nanchang, China.; 2 Department of Anesthesiology, the First Affiliated Hospital of Nanchang University, Nanchang, China., Ma LX; 2 Department of Anesthesiology, the First Affiliated Hospital of Nanchang University, Nanchang, China., Jiao C; 3 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, China., Kuang HX; 3 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, China., Zeng F; 4 Department of Pain Clinic, the First Affiliated Hospital of Nanchang University, Nanchang, China., Zhou XY; 3 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, China., Cheng XE; 2 Department of Anesthesiology, the First Affiliated Hospital of Nanchang University, Nanchang, China., Zhu MY; 4 Department of Pain Clinic, the First Affiliated Hospital of Nanchang University, Nanchang, China., Zhang DY; 4 Department of Pain Clinic, the First Affiliated Hospital of Nanchang University, Nanchang, China., Jiang CY; 5 Jisheng Han Academician Workstation for Pain Medicine, Nanshan Hospital, Shenzhen, China., Liu T; 1 Center for Experimental Medicine, the First Affiliated Hospital of Nanchang University, Nanchang, China.; 3 Department of Pediatrics, the First Affiliated Hospital of Nanchang University, Nanchang, China. |
| Abstrakt: |
Cav3 channels play an important role in modulating chronic pain. However, less is known about the functional changes of Cav3 channels in superficial spinal dorsal horn in neuropathic pain states. Here, we examined the effect of partial sciatic nerve ligation (PSNL) on either expression or electrophysiological properties of Cav3 channels in superficial spinal dorsal horn. Our in vivo studies showed that the blockers of Cav3 channels robustly alleviated PSNL-induced mechanical allodynia and thermal hyperalgesia, which lasted at least 14 days following PSNL. Meanwhile, PSNL triggered an increase in both mRNA and protein levels of Cav3.2 but not Cav3.1 or Cav3.3 in rats. However, in Cav3.2 knockout mice, PSNL predominantly attenuated mechanical allodynia but not thermal hyperalgesia. In addition, the results of whole-cell patch-clamp recordings showed that both the overall proportion of Cav3 current-expressing neurons and the Cav3 current density in individual neurons were elevated in spinal lamina II neurons from PSNL rats, which could not be recapitulated in Cav3.2 knockout mice. Altogether, our findings reveal that the elevated functional Cav3.2 channels in superficial spinal dorsal horn may contribute to the mechanical allodynia in PSNL-induced neuropathic pain model. |
