Synergistic enhancement of histamine release from rat peritoneal mast cells by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate is not reflected by corresponding changes in phospholipid turnover.

In an attempt to elucidate further the relationship between changes in phospholipid metabolism in, and histamine secretion from, purified rat peritoneal mast cells, the effects of the phorbol diester 12-O-tetradecanoylphorbol 13-acetate (TPA) on these responses in stimulated and unstimulated cells was investigated. TPA caused a dose-dependent increase in the incorporation of 32PO4(3-) into the mast cell phospholipids; phosphatidic acid (PA) and phosphatidylcholine (PC), but not phosphatidylinositol (PI). TPA synergistically enhanced histamine release from cells stimulated by anti-immunoglobulin E (IgE) and the calcium ionophore A23187, reducing its ED50 from 150 nM to 40 nM, but did not alter histamine release from cells stimulated by compound 48/80.

The hydrolysis of glycerophosphocholine by rat brain microsomes: activation and inhibition.

Experiments with glycerophosphocholine phosphodiesterase (GPC diesterase, EC 3.1.4.

Activation of glycerophosphocholine phosphodiesterase in rat forebrain by Ca2+.

The highest activity of glycerophosphocholine phosphodiesterase (EC 3.1.4.

The subcellular fractionation of the bovine caudate nucleus.

Two synaptosomal fractions could be obtained from bovine caudate nucleus on sucrose density gradients one of which had a much greater capacity for 'high affinity' choline uptake than the other but comparable amounts of CAT and choline kinase activity. Specific binding of QNB was widely distributed among all the subcellular fractions except the mitochondrial fraction and in quantitative terms by far the greatest amount was in the microsomal fraction. Only the microsomal fraction contained measurable amounts of glycerophosphocholine phosphodiesterase.