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Relationship Between the Actions of Calcium Ions, Opioids and Prostaglandin E 1 on the Level of Cyclic AMP in Neuroblastoma × Glioma Hybrid Cells
Author(s) -
Brandt M.,
Buchen C.,
Hamprecht B.
Publication year - 1980
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 - 10.1111/j.1471-4159.1980.tb11192.x
Subject(s) - prostaglandin e , egta , intracellular , chemistry , endocrinology , calcium , medicine , ionophore , calcium in biology , biochemistry , biology
Neuroblastoma × glioma hybrid cells increase their intracellular concentration of cyclic AMP in response to prostaglandin E 1 (PGE 1 ). This effect is inhibited by opioids. The response to PGE 1 is positively correlated with the concentration of Ca 2+ in the incubation medium. The Ca 2+ antagonists Co 2+ and La 3+ , the Ca 2+ chelator EGTA and a blocker of Ca 2+ influx into cells, Segontin, inhibit the response to PGE 1 . At low external concentrations of Ca 2+ the response to PGE 1 is enhanced by the Ca 2+ ionophore A23187. The effects of A23187 and Segontin point to a cytosolic site of Ca 2+ action. Lack of Ca 2+ reduces the level of cyclic AMP even in the absence of PGE 1 and the presence of an inhibitor of cyclic AMP phosphodiesterase. Ca 2+ is required even for an increase in the level of cyclic AMP in cells pretreated with cholera toxin. The increases in level of cyclic AMP evoked by PGE, in a neuroblastoma and by PGE 1 or noradrenaline in a glioma cell line do not depend on Ca 2+ . The response of the hybrid cells to the opioid leucine‐enkephalin appears not to rely on the presence of Ca 2+ . Even changing the intracellular concentration of Ca 2+ by the ionophore A23187 does not alter the effect of the opioid. The analogy between opioids and lack of Ca 2+ in the short‐term (minutes) experiments mentioned holds also for long‐term (hours) experiments. Cells chronically exposed to opioids or to low concentrations of Ca 2+ display an enhanced maximal response to PGE 1 .