Regulation of ion channel expression in neural cells by hormones and growth factors

1998 ◽  
Vol 18 (3) ◽  
pp. 175-225 ◽  
Author(s):  
Li-Jin Chew ◽  
Vittorio Gallo
Author(s):  
Ling-Ling Qian ◽  
Xiaojing Sun ◽  
Jingchun Yang ◽  
Xiao-Li Wang ◽  
Michael J. Ackerman ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0172884 ◽  
Author(s):  
Julia Pollak ◽  
Karan G. Rai ◽  
Cory C. Funk ◽  
Sonali Arora ◽  
Eunjee Lee ◽  
...  

2011 ◽  
Vol 100 (3) ◽  
pp. 284a
Author(s):  
Kaleef Williams ◽  
Jin O-Uchi ◽  
Angelica Martinez Perez ◽  
Coeli M.B. Lopes

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Muhammad Azhar Sherkheli ◽  
Guenter Gisselmann ◽  
Hanns Hatt

Transient receptor potential vanilloid subtype 3 (TRPV3) is a thermosensitive ion channel expressed in a variety of neural cells and in keratinocytes. It is activated by warmth (33–39°C), and its responsiveness is dramatically increased at nociceptive temperatures greater than 40°C. Monoterpenoids and 2-APB are chemical activators of TRPV3 channels. We found that Icilin, a known cooling substance and putative ligand of TRPM8, reversibly inhibits TRPV3 activity at nanomolar concentrations in expression systems likeXenopus laevesoocytes, HEK-293 cells, and in cultured human keratinocytes. Our data show that icilin's antagonistic effects for the warm-sensitive TRPV3 ion channel occurs at very low concentrations. Therefore, the cooling effect evoked by icilin may at least in part be due to TRPV3 inhibition in addition to TRPM8 potentiation. Blockade of TRPV3 activity by icilin at such low concentrations might have important implications for overall cooling sensations detected by keratinocytes and free nerve endings in skin. We hypothesize that blockage of TRPV3 might be a signal for cool-sensing systems (like TRPM8) to beat up the basal activity resulting in increased cold perception when warmth sensors (like TRPV3) are shut off.


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