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Bradykinin (BK) and its receptors, B 1 and B 2 , in trigeminal ganglion (TG) neurons are involved in the regulation of pain. Recent studies have revealed that B 1 receptors are expressed in neonatal rat TG neurons; however, the intracellular signaling pathway following B 1 receptor activation remains to be elucidated. To investigate the mechanism by which B 1 receptor activation leads to intracellular Ca 2+ mobilization, we measured the intracellular free Ca 2+ concentration ([Ca 2+ ] i ) in primary-cultured TG neurons. The application of Lys-[Des-Arg 9 ]BK (B 1 receptor agonist) increased the [Ca 2+ ] i in these TG neurons even in the absence of extracellular Ca 2+ . Pretreatment with inhibitors of ryanodine receptors or sarco/endoplasmic reticulum Ca 2+ -ATPase suppressed the increase in Lys-[Des-Arg 9 ]BK-induced [Ca 2+ ] i . The Lys-[Des-Arg 9 ]BK-induced [Ca 2+ ] i increase was unaffected by phospholipase-C inhibitor. B 1 receptor activation-induced [Ca 2+ ] i increase was suppressed by phosphodiesterase inhibitor and enhanced by adenylyl cyclase inhibitor. These results suggest that B 1 receptor activation suppresses intracellular cAMP production via adenylyl cyclase inhibition and mobilizes intracellular Ca 2+ via ryanodine receptors that access intracellular Ca 2+ stores.

Intracellular Ca2+ mobilization pathway via bradykinin B1 receptor activation in rat trigeminal ganglion neurons