Wogonin Inhibits LPS-Induced Inflammatory Responses in Rat Dorsal Root Ganglion Neurons Via Inhibiting TLR4–MyD88–TAK1-Mediated NF-κB and MAPK Signaling Pathway

2014 ◽  
Vol 35 (4) ◽  
pp. 523-531 ◽  
Author(s):  
Shibiao Chen ◽  
Jiangqin Xiong ◽  
Yanping Zhan ◽  
Weicheng Liu ◽  
Xiuhong Wang
Keyword(s):  
Dorsal Root Ganglion ◽  
Signaling Pathway ◽  
Dorsal Root ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

5HT Increases Excitability of Nociceptor-Like Rat Dorsal Root Ganglion Neurons Via cAMP-Coupled TTX-Resistant Na+Channels

2001 ◽  
Vol 86 (1) ◽  
pp. 241-248 ◽  
Author(s):  
Luz M. Cardenas ◽  
Carla G. Cardenas ◽  
Reese S. Scroggs
Keyword(s):  
Dorsal Root Ganglion ◽  
Signaling Pathway ◽  
Dorsal Root ◽  
Phosphodiesterase Inhibitor ◽  
Dorsal Root Ganglion Neurons ◽  
Receptor Coupling ◽  
Low Threshold ◽  
Ganglion Neurons ◽  
Serotonergic Modulation

The physiological effects of 5HT receptor coupling to TTX-resistant Na+ current, and the signaling pathway involved, was studied in a nociceptor-like subpopulation of rat dorsal root ganglion (DRG) cells (type 2), which can be identified by expression of a low-threshold, slowly inactivating A-current. The 5HT-mediated increase in TTX-resistant Na+ current in type 2 DRG cells was mimicked and occluded by 10 μM forskolin. Superfusion of type 2 DRG cells on the outside with 1 mM 8-bromo-cAMP or chlorophenylthio-cAMP (CPT-cAMP) increased the Na+ current, but less than 5HT itself. However, perfusion of the cells inside with 2 mM CPT-cAMP strongly increased the amplitude of control Na+currents and completely occluded the effect of 5HT. Thus it appears that the signaling pathway includes cAMP. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine (200 μM) also mimicked the effect of 5HT on Na+ current, suggesting tonic adenylyl cyclase activity. 5HT reduced the amount of current required to evoke action potentials in type 2 DRG cells, suggesting that 5HT may lower the threshold for activation of nociceptor peripheral receptors. The above data suggest that serotonergic modulation of TTX-resistant Na+channels through a cAMP-dependent signaling pathway in nociceptors may participate in the generation of hyperalgesia.

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