Premium
Signal Flows from Two Phospholipase C‐Linked Receptors Are Independent in PC12 Cells
Author(s) -
Suh ByungChang,
Lee ChinOk,
Kim KyongTai
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64031071.x
Subject(s) - phospholipase c , extracellular , purinergic receptor , receptor , second messenger system , homologous desensitization , inositol , intracellular , secretion , inositol phosphate , inositol trisphosphate , microbiology and biotechnology , chemistry , inositol trisphosphate receptor , fura 2 , biology , endocrinology , medicine , agonist , biochemistry , cytosol , enzyme
Bradykinin (BK) receptor and P 2 ‐purinergic receptor are known to be coupled to phospholipase C (PLC) in PC12 cells. To study the interaction between these two PLC‐linked receptors, the presence of both receptors on individual cells was demonstrated by sequential Ca 2+ spikes caused by BK and ATP in a single fura‐2‐loaded cell. BK‐ and ATP‐induced catecholamine (CA) secretions were desensitized within 5 min. However, in the sequential experiment, the BK‐induced homologous desensitization of CA secretion did not block the ATP‐induced secretion, and vice versa. Each agonist‐induced an increase in inositol 1,4,5‐trisphosphate (IP 3 ) production and intracellular free Ca 2+ concentration also led to homologous desensitization. However, there was no heterologous desensitization between the two agonists. When the cells were treated with both BK and ATP simultaneously, the amounts of CA secretion, IP 3 production, internal Ca 2+ mobilization, and Ca 2+ influx were all additive. We also found that both IP 3 ‐induced Ca 2+ release from intracellular Ca 2+ stores and Ca 2+ influx from extracellular space were able to release [ 3 H]norepinephrine, and the secretion induced by both agonists was exactly additive in the absence or presence of extracellular Ca 2+ . The data suggest that the CA secretions caused by BK or ATP may have separate secretory pathways even though they activate identical second messenger pathways.