THE ROLE OF LIPIDS IN THE OBSERVED LACK OF PHOSPHATIDYLCHOLINE EXCHANGE IN MYELIN

Abstract— When exchange between liposomal phosphatidylcholine and that in a whole myelin fraction from guinea-pig brain was studied, very little exchange was observed. In order to investigate the reason for this phenomenon, myelin lipids in the Ca²⁺ form were prepared and subjected to sonication under the same conditions usually used to study phosphatidylcholine exchange. Despite the high cholesterol content in these extracts, this treatment produced liposomes of a size (12 nm Stoke's radius) similar to that of pure phosphatidylcholine liposomes. In this form, myelin total lipids were capable of undergoing exchange, and this was only demonstrable in the fraction containing phosphatidylcholine and that containing phosphatidylinositol. Since the level of acidic phospholipids in these total lipid extracts is potentially capable of producing 40% inhibition of phosphatidylcholine exchange (H ellings et al , 1974; B rammer & S heltawy , 1975), control experiments were carried out to ensure that the observed phosphatidylcholine exchange in the myelin lipid extract was not due to the loss of phosphoinositides. This was found to be the case, and it was concluded therefore that total myelin lipids, in the Ca²⁺ form, are capable of phosphatidylcholine exchange and that the observed lack of it in the whole myelin is due either to the effect of myelin proteins or the compact structure of the myelin membrane.
Calculations based on the difference between the rate of phosphatidylcholine exchange in the myelin liposomes and in the sonicated phosphatidylcholine liposomes indicated that the phosphatidylcholine is asymmetrically distributed in the myelin liposomes. Almost all the phosphatidylcholine seems to be present in the outer half of the bilayer.