STUDIES OF THE CATIONIC, AND ACETYLCHOLINE, STIMULATION OF PHOSPHATE INCORPORATION INTO PHOSPHOLIPIDS IN RAT BRAIN CORTEX IN VITRO

Abstract

The addition of 0.1 M KCl to, or the omission of CaCl2from, incubation media in which rat brain cortex slices are respiring, stimulates the incorporation of inorganic P32into phospholipids. It also stimulates the labelling of 7-minute hydrolyzable nucleotide phosphates, but decreases their levels. The stimulation of P32incorporation into total phospholipid takes place primarily into phosphatidic acid and phosphoinositide but not into phosphatidyl choline and phosphatidyl ethanolamine. The addition of succinate and γ-aminobutyrate to brain cortex slices, metabolizing glucose, markedly inhibits the labelling of phospholipids although the respiration of slices is not diminished. The potassium stimulation of phospholipid labelling only occurs if sodium ions are present in the incubation medium. The lesser stimulation due to absence of calcium ions seems, however, to be independent of the presence of sodium ions. Acetylcholine stimulation of P32incorporation into phospholipids is dependent on the presence of sodium ions. Such stimulations are suppressed by concentrations of malonate, iodoacetate, fluoride, and ethanol that have little effect on the unstimulated incorporation of P32. Atropine and hyoscine inhibit acetylcholine stimulation but not cationic stimulation of P32incorporation. It is suggested that the effect of acetylcholine on P32incorporation is mediated by cationic changes at the nerve cell membrane.