Sustained Ca super(2+) signaling in mouse lacrimal acinar cells due to photolysis of "caged" glycerophosphoryl-myo-inositol 4,5-bisphosphate

In saponin-permeabilized mouse lacrimal acinar cells, glycerophosphoryl-myo-inositol 4,5-bisphosphate (GPIP sub(2)) activated the release of sequestered Ca super(2+) to the same extent as inositol 1,4,5-trisphosphate ((1,4,5)IP sub(3)) but with a potency about 1/10 that of (1,4,5)IP sub(3). In lacrimal gland homogenates, ( super(3)H)GPIP sub(2) was metabolized to two compounds which upon anion exchange high performance liquid chromatography eluted at positions indicating that they were ( super(3)H)GPIP and ( super(3)H)GPIP sub(3). The rate of metabolism of ( super(3)H)GPIP sub(2) was much slower than that of ( super(3)H)(1,4,5)IP sub(3), and its rate of phosphorylation was less than 1% of that of ( super(3)H)(1,4,5)IP sub(3). In intact lacrimal cells, photolysis of a microinjected "caged" derivative of GPIP sub(2), 1-( alpha -glycerophosphoryl)-myo-inositol 4,5-bisphosphate P super(4(5))-1-(2-nitrophenyl)ethyl ester, resulted in sustained activation of Ca super(2+) signaling; i.e. intracellular Ca super(2+) release followed by increased entry of Ca super(2+) across the plasma membrane.