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

Abstract

Phosphatidylserine, which is necessary for protein kinase C activity, is synthesized in mammalian tissues by the Ca²⁺-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 mechanisms for phosphatidylserine synthesis is established during development and that N₂-treatment can increase phosphatidylserine synthesis by interfering with this regulatory mechanism.