Phosphatidylcholine metabolism was examined in neonatal mouse calvaria in vitro. Incorporation of choline into phosphatidylcholine was slow in this tissue. At 2 h after a pulse of [methyl-3H]choline only 30% of the tissue radioactivity was in the organic phase. Chromatography of the aqueous phase of the tissue extract revealed that more than half of the radioactivity was present as choline at this time. There was no accumulation of phosphocholine, which would have been expected if the cytidylyltransferase were the rate-limiting step in the CDP-choline pathway in the tissue. Choline kinase activity in calvarial cytosol was lower than choline kinase activity in liver cytosol of the same animals. No evidence for significant phosphatidylcholine synthesis through the methylation pathway was found in the calvarial tissue. Although rates of choline-phosphatidylcholine base exchange were higher in bone microsomes than in microsomes from liver, the rate of phosphatidylcholine production through this pathway appeared to be too slow to account for the phosphatidylcholine produced by the calvaria. Phosphatidylcholine synthesis in the calvaria was unaffected by 2 h of treatment with 10 nM-parathyroid hormone, 0.1 nM-0.1 microM-1 alpha,25-dihydroxycholecalciferol, 5 microM-prostaglandin E1 or 2.5 nM-salmon calcitonin, or by 17 h of treatment with 10 nM-parathyroid hormone or 0.1 nM-1 alpha,25-dihydroxycholecalciferol.
.GAMMA.-Pyrones from Gonystylus keithii, as New Inhibitors of Parathyroid Hormone (PTH)-Induced Ca Release from Neonatal Mouse Calvaria.