Effects of prostaglandin E2 and progesterone on rat brain synaptosomal plasma membranes.

The lipid fluidity of rat brain synaptosomal plasma membranes (SPM) labelled with 1,6-diphenyl-1,3,5-hexatriene (DPH) was increased by prostaglandin E2 (PGE2) and decreased by progesterone, as indicated by steady-state fluorescence anisotropy [(ro/r)-1]-1. Arrhenius-type plots of [(ro/r)-1]-1 indicated a lipid phase separation of SPM at approximately 23.5 degrees C which was reduced to approximately 18.1 degrees C by PGE2 and increased to approximately 34.6 degrees C by progesterone. Treatment of SPM by PGE2 and progesterone caused an increase of the lipid phase separation to approximately 32.4 degrees C. Arrhenius plots of Na+/K(+)-ATPase activity in control SPM exhibited a break point at approximately 23.1 degrees C which was reduced to approximately 17.8 degrees C by PGE2 and increased to approximately 32.6 degrees C by progesterone. SPM treated with PGE2 plus progesterone showed an increased break point at approximately 29.3 degrees C. Na+/K(+)-ATPase activity was increased at a PGE2 concentration range between 0.1 and 3 microM; higher concentrations (up to 10 microM) led to a gradual inhibition of enzyme activity. Progesterone (0.1-10 microM) and PGE2 plus progesterone both produced a gradual decrease in enzyme activity. The allosteric inhibition of Na+/K(+)-ATPase by fluoride (F-) (as reflected by changes in the Hill coefficient) was modulated by PGE2 and progesterone. The perturbations of membrane lipid structure and changes in membrane fluidity provide a basis for suggesting an independent non-genomic mechanism for the progesterone-induced alterations in the effects of PGE2 on brain function.