scholarly journals Bradykinin inhibits M current via phospholipase C and Ca2+ release from IP3-sensitive Ca2+ stores in rat sympathetic neurons

1998 ◽  
Vol 95 (12) ◽  
pp. 7151-7156 ◽  
Author(s):  
H. Cruzblanca ◽  
D.-S. Koh ◽  
B. Hille
BIOS ◽  
2010 ◽  
Vol 81 (2) ◽  
pp. 55-61
Author(s):  
Rebecca Riblet ◽  
Amanpreet Kaur ◽  
Harleen Kaur ◽  
Mark D. Womble

1996 ◽  
Vol 207 (2) ◽  
pp. 97-100 ◽  
Author(s):  
Takayuki Tokimasa ◽  
Mark A. Simmons ◽  
Carla R. Schneider ◽  
Takashi Akasu

2000 ◽  
Vol 285 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Susumu Kotani ◽  
Takae Hirasawa ◽  
Tomotaro Suzuki ◽  
Kazunori Sato ◽  
Manabu Sakakibara ◽  
...  

2020 ◽  
Vol 21 (16) ◽  
pp. 5796
Author(s):  
Paula Rivas-Ramírez ◽  
Antonio Reboreda ◽  
Lola Rueda-Ruzafa ◽  
Salvador Herrera-Pérez ◽  
Jose Antonio Lamas

The ionic mechanisms controlling the resting membrane potential (RMP) in superior cervical ganglion (SCG) neurons have been widely studied and the M-current (IM, KCNQ) is one of the key players. Recently, with the discovery of the presence of functional TREK-2 (TWIK-related K+ channel 2) channels in SCG neurons, another potential main contributor for setting the value of the resting membrane potential has appeared. In the present work, we quantified the contribution of TREK-2 channels to the resting membrane potential at physiological temperature and studied its role in excitability using patch-clamp techniques. In the process we have discovered that TREK-2 channels are sensitive to the classic M-current blockers linopirdine and XE991 (IC50 = 0.310 ± 0.06 µM and 0.044 ± 0.013 µM, respectively). An increase from room temperature (23 °C) to physiological temperature (37 °C) enhanced both IM and TREK-2 currents. Likewise, inhibition of IM by tetraethylammonium (TEA) and TREK-2 current by XE991 depolarized the RMP at room and physiological temperatures. Temperature rise also enhanced adaptation in SCG neurons which was reduced due to TREK-2 and IM inhibition by XE991 application. In summary, TREK-2 and M currents contribute to the resting membrane potential and excitability at room and physiological temperature in the primary culture of mouse SCG neurons.


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