Phosphatidylserine synthesis in rat cerebral cortex: effects of hypoxia, hypocapnia and development

Phosphatidylserine, which is necessary for protein kinase C activity, is synthesized in mammalian tissues by the Ca(2+)-dependent base exchange enzyme. The synthesis of phosphatidylserine is greater in slices or homogenates of rat cerebral cortex subjected to hypoxia by N2 treatment when compared with O2 plus 5% CO2. An intermediate effect was observed when the treatment was done with N2 plus 5% CO2. Incorporation rates were dependent on Ca2+ in Krebs-Henseleit Ringer bicarbonate medium, being greater with 2 mM Ca2+ than with the same medium prepared without Ca2+. The increase of phosphatidylserine synthesis, due to hypoxia, was, on the contrary, more evident in the medium lacking added Ca2+. Similar results were obtained with the homogenates. This suggests that elevation of intracellular Ca2+, caused by hypocapnia and hypoxia, may be responsible for the greater incorporation of serine into phosphatidylserine. In both cerebrocortical slices and homogenate, [14C]serine incorporation decreased with development both in O2 plus 5% CO2 and N2-treated preparations. However, in younger rats (14-18 days) hypoxia induced a lesser increase of phosphatidylserine than in 40 day old animals. We suggest that a regulatory mechanism for phosphatidylserine synthesis is established during development and that N2-treatment can increase phosphatidylserine synthesis by interfering with this regulatory mechanism.