Sulfur dioxide derivatives modulation of high-threshold calcium currents in rat dorsal root ganglion neurons

被引:6
作者
Du, Zhengqing [1 ]
Meng, Ziqiang
机构
[1] Shanxi Univ Finance & Econ, Taiyuan 030006, Peoples R China
[2] Shanxi Univ, Inst Environm Med & Toxicol, Taiyuan 030006, Peoples R China
关键词
sulfur dioxide derivatives; high-voltage-activated calcium currents (HVA-I-Ca); whole-cell patch clamp; dorsal root ganglion; SODIUM CURRENTS; LIPID-PEROXIDATION; SENSORY NEURONS; CA2+ CHANNEL; MICE; SUBUNIT; MECHANISMS; ALLODYNIA; BISULFITE; ORGANS;
D O I
10.1016/j.neulet.2006.06.046
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This study addressed the effect of sulfur dioxide (SO2) derivatives on high-voltage-activated calcium currents (HVA-I-Ca) in somatic membrane of freshly isolated rat dorsal root ganglion (DRG) neurons by using the whole-cell configuration of patch-clamp technique. High-threshold Ca2+ channels are highly expressed in small dorsal root ganglion neurons. SO2 derivatives increased the amplitudes of calcium currents in a concentration-dependent and voltage-dependent manner. The 50% enhancement concentrations (EC50) of SO2 derivatives on HVA-I-Ca was about 0.4 mu M. In addition, SO2 derivatives significantly shifted the activation and inactivation curve in the depolarizing direction. Parameters for the fit of a Boltzmann equation to mean values for the activation were V-1/2 = -17.9 +/- 1.3 mV before and -12.5 +/- 1.1 mV after application 0.5 mu M SO2 derivatives 2 min (P < 0.05). The half inactivation of HVA-I-Ca was shifted 9.7 mV to positive direction (P < 0.05). Furthermore, SO2 derivatives significantly prolonged the slow constant of inactivation, slowed the fast recovery but markedly accelerated the slow recovery of HVA-I-Ca from inactivation. From HP of -60 mV 0.5 mu M SO2 derivatives increased the amplitude of HVA-I-Ca with a depolarizing voltage step to -10 mV about 54.0% in small DRG neurons but 33.3% in large DRG neurons. These results indicated a possible correlation between the change of calcium channels and SO, inhalation toxicity, which might cause periphery neurons abnormal regulation of nociceptive transmission via calcium channels. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:147 / 152
页数:6
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