Regulation of histamine H1 receptor-mediated phosphoinositide hydrolysis by histamine and phorbol esters in DDT1 MF-2 cells

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Abstract

The regulation of histamine-stimulated phosphoinositide turnover by histamine and phorbol esters was examined in intact DDT1 MF-2 cells grown in suspension culture. Histamine increased the incorporation of 32P into phosphatidylinositol (PI) in these cells, and this stimulation was inhibited by the H1 antagonist diphenhydramine but not by the H2 antagonist cimetidine. Pretreatment of cells with histamine or with phorbol 12-myristate 13-acetate (PMA) or other activators of protein kinase C induced a marked decrease in the subsequent stimulation by histamine. PMA, but not histamine, also decreased the ability of epinephrine to stimulate PI labelling through α1-adrenoceptors. Thus, histamine appears to induce homologous desensitization of histamine H1 receptor-mediated PI turnover, whereas direct activation of protein kinase C in the absence of receptor occupancy by agonist induces nonspecific heterologous desensitization of both histamine H1- and α1-adrenoceptor-mediated responses.

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      Histamine-induced IP1 accumulation in C6 glioma cells with an EC50 of 4.2 μM caused more than an 11-fold increase over the basal level at maximal response of 100 μM histamine. The EC50 value obtained in this study is comparable with that of related glial cells and other cells used in the previous studies, such as U373 MG astrocytoma (EC50 = 5.4 μM),24 DDT1 MF-2 (EC50 = 10 μM),25 astrocyte-enriched primary culture (EC50 = 1.7 μM),13 oligodendroglioma (EC50 = 1.6 μM),26 and C6 glioma cells (EC50 = 24 μM5). Histamine-induced transient [Ca2+]i increase, with an EC50 of 4.9 μM, was higher than its sustained [Ca2+]i increase, with EC50 of 0.63 μM.

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