[Effect of corticotropin on the rate of 32P-orthophosphate incorporation into the synaptosome phosphoinositides of the ischemic rat brain].

A high rate of 32P turnover in polyphosphoinositides (up to 80% of the total radioactivity) was found in synaptosomes of normal and ischemic rat brain. Corticotropin (ACTH) increases the rate of 32P turnover in polyphosphoinositides of normal synaptosomes and decreases it in ischemic synaptosomes. Depolarization (high KCl concentration in the incubation medium) activates polyphosphoinositide metabolism in normal (by 50%) and ischemic (by 30%) synaptosomes. The combined influence of depolarization and ACTH results in the additive effect. Thus, a stimulating effect of ACTH on phosphoinositide metabolism disturbed in ischemia was recovered during depolarization of ischemic synaptosomes.