The effect of botulinum neurotoxin type A on Nav1.3 sodium channels and sodium currents in animals modeling neuropathic pain
10.3760/cma.j.issn.0254-1424.2020.09.001
- VernacularTitle:A型肉毒毒素对神经病理性疼痛大鼠钠离子通道Nav1.3和钠电流的影响
- Author:
Xi CHEN
1
;
Yuhan YANG
;
Qing CAI
;
Sen LIANG
;
Xiquan HU
Author Information
1. 中山大学附属第三医院康复医学科，广州 510630
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2020;42(9):769-774
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of botulinum neurotoxin type A (BoNT/A) on Nav1.3 sodium channels and the function of sodium current in neuropathic pain.Methods:Eighteen adult rats had a spared nerve injury (SNI) induced and then were randomly divided into a saline group and a BoNT/A group, each of 9. Another 9 rats formed a fake operation group, Five days after the SNI, BoNT/A (7U/kg or 15U/kg) or saline was subcutaneously administered into the plantar surface of a hindpaw. On the 3rd, 7th and 14th day after the injection, the SNI rats′ paw withdrawal threshold was measured. On the 7th and 14th day the expression of Nav1.3 protein in dorsal root ganglion (DRG) neurons was examined using western blotting, while any change in the functional tetrodotoxin-sensitive (TTX-S) current was recorded using the patch clamp technique.Results:Administration of BoNT/A at either 7U/kg or 15U/kg significantly increased the SNI-induced mechanical allodynia. The expression of Nav1.3 protein in DRG neurons increased significantly after the SNI, but had decreased significantly by the 7th and 14th day after the administration of BoNT/A. BoNT/A significantly decreased the current density in TTX-S sodium channels in DRG neurons following SNI.Conclusion:Administration of BoTN/A affects the expression of Nav1.3 protein and functional TTX-S current, relieving neuropathic pain.
