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J. Biol. Chem., Vol. 266, Issue 33, 22234-22241, Nov, 1991
RJ Wojcikiewicz and SR Nahorski
The possibility that chronic activation of the phosphoinositide- mediated
signaling pathway modifies the Ca(2+)-mobilizing action of inositol
1,4,5-trisphosphate (InsP3) was examined. SH-SY5Y human neuroblastoma cells
were exposed to carbachol, permeabilized electrically, loaded with 45Ca2+,
and 45Ca2+ mobilization in response to exogenous InsP3 was assessed. In
control permeabilized cells, InsP3 released 65 +/- 2% of sequestered 45Ca2+
(EC50 = 0.32 +/- 0.05 microM). Pre-treatment with carbachol reduced both
maximal InsP3-induced 45Ca2+ release (to 34 +/- 3%, with half-maximal and
maximal inhibition at approximately 3 and 6 h, respectively) and the
potency of InsP3 (EC50 = 0.92 +/- 0.13 microM). This inhibitory effect of
carbachol was half- maximal at approximately 5 microM, was mediated by
muscarinic receptors, and was reversible following withdrawal of agonist.
Pretreatment with phorbol 12,13-dibutyrate did not alter the maximal effect
of InsP3 but doubled its EC50. Evidence suggesting that the inhibitory
effects of carbachol pretreatment resulted from altered Ca2+ homeostasis
was not forthcoming; both 45Ca2+ uptake and release induced by ionomycin
and thapsigargin were identical in control and pretreated permeabilized
cells, as were the characteristics of reuptake of released Ca2+. In
contrast, carbachol pretreatment, without altering the affinity of InsP3
(Kd = 64 +/- 7 nM), reduced the density of [32P]InsP3-binding sites from
2.0 +/- 0.1 to 1.0 +/- 0.1 pmol/mg protein with a time course essentially
identical to that for the reduction in responsiveness to InsP3. This effect
was not mimicked by pretreatment of cells with phorbol 12,13-dibutyrate.
These data indicate that chronic activation of phosphoinositide hydrolysis
can reduce the abundance of InsP3 receptors and that this causes a
reduction in size of the InsP3-sensitive Ca2+ store. This modification,
possibly in conjunction with a protein kinase C-mediated event, appears to
account for the carbachol-induced suppression of InsP3 action. As
intracellular InsP3 mass remained elevated above basal for at least 24 h
after addition of carbachol, suppression of the Ca(2+)-mobilizing activity
of InsP3 represents an important adaptive response to cell stimulation that
can limit the extent to which intracellular Ca2+ is mobilized.
Chronic muscarinic stimulation of SH-SY5Y neuroblastoma cells suppresses inositol 1,4,5-trisphosphate action. Parallel inhibition of inositol 1,4,5-trisphosphate-induced Ca2+ mobilization and inositol 1,4,5-trisphosphate binding
Department of Pharmacology and Therapeutics, University of Leicester, United Kingdom.
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