Up-Regulation of NaV1.7 Sodium Channels Expression by Tumor Necrosis Factor-α in Cultured Bovine Adrenal Chromaffin Cells and Rat Dorsal Root Ganglion Neurons

2014 ◽  
Vol 118 (2) ◽  
pp. 318-324 ◽  
Author(s):  
Ryuji Tamura ◽  
Takayuki Nemoto ◽  
Toyoaki Maruta ◽  
Shin Onizuka ◽  
Toshihiko Yanagita ◽  
...  
Keyword(s):  
Sodium Channels ◽  
Dorsal Root ◽  
Chromaffin Cells ◽  
Tumor Necrosis ◽  
Dorsal Root Ganglion Neurons ◽  
Adrenal Chromaffin Cells ◽  
Adrenal Chromaffin ◽  
Ganglion Neurons ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Modulation of Voltage-Gated Sodium Channels by Activation of Tumor Necrosis Factor Receptor-1 and Receptor-2 in Small DRG Neurons of Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
M. Leo ◽  
S. Argalski ◽  
M. Schäfers ◽  
T. Hagenacker
Keyword(s):  
Tumor Necrosis Factor ◽  
Sodium Channels ◽  
Tumor Necrosis ◽  
Dorsal Root Ganglion Neurons ◽  
Maximum Effect ◽  
Tnf Receptor ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Ganglion Neurons ◽  
Necrosis Factor

Tumor necrosis factor- (TNF-)αis a proinflammatory cytokine involved in the development and maintenance of inflammatory and neuropathic pain. Its effects are mediated by two receptors, TNF receptor-1 (TNFR-1) and TNF receptor-2 (TNFR-2). These receptors play a crucial role in the sensitization of voltage-gated sodium channels (VGSCs), a key mechanism in the pathogenesis of chronic pain. Using the whole-cell patch-clamp technique, we examined the influence of TNFR-1 and TNFR-2 on VGSCs and TTX-resistant NaV1.8 channels in isolated rat dorsal root ganglion neurons by using selective TNFR agonists. The TNFR-1 agonist R32W (10 pg/mL) caused an increase in the VGSC current (INa(V)) by 27.2 ± 5.1%, while the TNFR-2 agonist D145 (10 pg/mL) increased the current by 44.9 ± 2.6%. This effect was dose dependent. Treating isolated NaV1.8 with R32W (100 pg/mL) resulted in an increase inINaV(1.8)by 18.9 ± 1.6%, while treatment with D145 (100 pg/mL) increased the current by 14.5 ± 3.7%. Based on the current-voltage relationship, 10 pg of R32W or D145 led to an increase inINa(V)in a bell-shaped, voltage-dependent manner with a maximum effect at −30 mV. The effects of TNFR activation on VGSCs promote excitation in primary afferent neurons and this might explain the sensitization mechanisms associated with neuropathic and inflammatory pain.

scholarly journals Protein Kinase C-α and -ε Down-Regulate Cell Surface Sodium Channels via Differential Mechanisms in Adrenal Chromaffin Cells

2002 ◽  
Vol 74 (4) ◽  
pp. 1674-1684 ◽  
Author(s):  
Toshihiko Yanagita ◽  
Hideyuki Kobayashi ◽  
Ryuichi Yamamoto ◽  
Hiroaki Kataoka ◽  
Hiroki Yokoo ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Surface ◽  
Sodium Channels ◽  
Chromaffin Cells ◽  
Adrenal Chromaffin Cells ◽  
Kinase C ◽  
Adrenal Chromaffin
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