Intracellular Ca 2+ mobilization pathway via bradykinin B 1 receptor activation in rat trigeminal ganglion neurons

The journal of physiological sciences

article

Reiko Terashima¹  Maki Kimura²  Asuka Higashikawa²  Yuki Kojima²  Tatsuya Ichinohe¹  Masakazu Tazaki²  Yoshiyuki Shibukawa² 

[1] Department of Dental Anesthesiology, Tokyo Dental College;Department of Physiology, Tokyo Dental College

关键词: Adenylyl cyclase;    Ca 2+ mobilization;    Cyclic AMP;    G protein;    Ryanodine receptors;    Trigeminal ganglion neuron;   

DOI  :  10.1007/s12576-018-0635-3

来源: Springer

【 摘 要 】

Bradykinin (BK) and its receptors, B1 and B2, in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B1 receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B1 receptor activation remains to be elucidated. To investigate the mechanism by which B1 receptor activation leads to intracellular Ca2+ mobilization, we measured the intracellular free Ca2+ concentration ([Ca2+]i) in primary-cultured TG neurons. The application of Lys-[Des-Arg9]BK (B1 receptor agonist) increased the [Ca2+]i in these TG neurons even in the absence of extracellular Ca2+. Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca2+-ATPase suppressed the increase in Lys-[Des-Arg9]BK-induced [Ca2+]i. The Lys-[Des-Arg9]BK-induced [Ca2+]i increase was unaffected by phospholipase-C inhibitor. B1 receptor activation-induced [Ca2+]i increase was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B1 receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca2+ via ryanodine receptors that access intracellular Ca2+ stores.

【 授权许可】

Unknown