Cholinergic modulation of the Ca2+ response to bradykinin in neuroblastoma cells

• DOI: 10.1152/ajpcell.1997.273.2.c612
• Publication Date: 2017-12-24T16:07:55Z
• Authors: J. S. Coggan; S. H. Thompson
• Keywords: Homologous desensitization; Inositol trisphosphate

Fura 2 imaging was used to measure intracellular Ca2+ signals in N1E-115 mouse neuroblastoma cells during combined activation of bradykinin (BK) and cholinergic receptors. BK carbachol (CCh) both activate phospholipase C (PLC) cause release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores. The signal response CCh is prolonged by the influx, but does not appear influx pathway. When are applied together (BK+CCh), composed influx. also activated BK+CCh a subset that respond with concentration increase when presented itself. This suggests stimulates Ca(2+)-silent receptor coupled acts synergistically receptors Pertussis toxin reduces without affecting release, indicating G protein modulates pathway different responsible for activating PLC. Cholinergic stimulation causes progressive heterologous desensitization BK-evoked release. Desensitization has unique property continuing develop after agonist removed fully recovered. Heterologous result store depletion or long-lasting inhibition PLC IP3-dependent Instead, it appears involve an early step BK-signaling cascade, possibly at level B2 associated proteins.