GABA-mediated modulation of ATP-induced intracellular calcium responses in nodose ganglion neurons of the rat

2015 ◽  
Vol 584 ◽  
pp. 168-172 ◽  
Author(s):  
Takuya Yokoyama ◽  
Shou Fukuzumi ◽  
Hitomi Hayashi ◽  
Nobuaki Nakamuta ◽  
Yoshio Yamamoto
2007 ◽  
Vol 52 (3) ◽  
pp. 904-924 ◽  
Author(s):  
Shigeji Matsumoto ◽  
Shinki Yoshida ◽  
Mizuho Ikeda ◽  
Takeshi Tanimoto ◽  
Chikako Saiki ◽  
...  

Gene ◽  
1997 ◽  
Vol 202 (1-2) ◽  
pp. 7-14 ◽  
Author(s):  
Jun Chen ◽  
Stephen R Ikeda ◽  
Wenhua Lang ◽  
Carlos M Isales ◽  
Xiangyang Wei

2009 ◽  
pp. NA-NA
Author(s):  
Hui-ya Hsieh ◽  
Carolyn L. Robertson ◽  
Anke Vermehren-Schmaedick ◽  
Agnieszka Balkowiec

PLoS ONE ◽  
2018 ◽  
Vol 13 (6) ◽  
pp. e0199282 ◽  
Author(s):  
Diego Fernández-Fernández ◽  
Alba Cadaveira-Mosquera ◽  
Lola Rueda-Ruzafa ◽  
Salvador Herrera-Pérez ◽  
Emma L. Veale ◽  
...  

1997 ◽  
Vol 77 (6) ◽  
pp. 3391-3395 ◽  
Author(s):  
Chaoying Li ◽  
Robert W. Peoples ◽  
Forrest F. Weight

Li, Chaoying, Robert W. Peoples, and Forrest F. Weight. Mg2+ inhibition of ATP-activated current in rat nodose ganglion neurons: evidence that Mg2+ decreases the agonist affinity of the receptor. J. Neurophysiol. 77: 3391–3395, 1997. The effect of Mg2+ on ATP-activated current in rat nodose ganglion neurons was investigated with the use of the whole cell patch-clamp technique. Mg2+ decreased the amplitude of ATP-activated current in a concentration-dependent manner over the concentration range of 0.25–8 mM, with a 50% inhibitory concentration value of 1.5 mM for current activated by 10 μM ATP. Mg2+ shifted the ATP concentration-response curve to the right in a parallel manner, increasing the 50% effective concentration value for ATP from 9.2 μM in the absence of added Mg2+ to 25 μM in the presence of 1 mM Mg2+. Mg2+ increased the deactivation rate of ATP-activated current without changing its activation rate. The observations are consistent with an action of Mg2+ to inhibit ATP-gated ion channel function by decreasing the affinity of the agonist binding site on these receptors.


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