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Title: Complex relationship between Ins(1,4,5)P3 accumulation and Ca2+ -signalling in a human neuroblastoma reveled by cellular differentiation.
Authors: Martin, AK
Nahorski, SR
Willars, GB
First Published: Apr-1999
Citation: BR J PHARMACOL, 1999, 126 (7), pp. 1559-1566
Abstract: 1. Differentiation of SH-SY5Y neuroblastoma cells induces morphological and biochemical changes consistent with a more neuronal phenotype. These cells may therefore provide a model for studying phenomena such as signal transduction in a neuronal context whilst retaining the advantages of a homogenous cell population expressing a well characterized array of G-protein coupled receptors. 2. This study examined the effects of differentiating SH-SY5Y cells on muscarinic- and bradykinin-receptor-mediated phosphoinositide and Ca2+ signalling. Retinoic acid (10 microM, 6 days) along with a lowered serum concentration produced phenotypic changes consistent with differentiation including reduced proliferation and increased neurite outgrowth. 3. Differentiation increased the magnitude and potency of rapid Ins(1,4,5)P3 responses to a full muscarinic receptor agonist. Bradykinin receptor-mediated Ins(1,4,5)P3 signalling was also potentiated following differentiation. Determination of agonist-evoked accumulation of [3H]-inositol phosphates under lithium-block demonstrated these changes reflected enhanced phospholipase C activity which is consistent with observed increases in the expression of muscarinic and bradykinin receptors. 4. Despite the marked alterations in Ins(1,4,5)P3 signalling following differentiation, elevations of intracellular [Ca2+] were totally unaltered. Thus, in SH-SY5Y cells, the relationship between the elevations of Ins(1,4,5)P3 and intracellular [Ca2+] is agonist dependent and affected by the state of differentiation. This demonstrates that mechanisms other than the measured increase in Ins(1,4,5)P3 regulate the elevation of intracellular [Ca2+].
DOI Link: 10.1038/sj.bjp.0702464
ISSN: 0007-1188
Type: Journal Article
Appears in Collections:Published Articles, Dept. of Cell Physiology and Pharmacology

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