Role of the phosphoinositide signal system and methylation of phosphatidylethanolamine in the development of long-term post-tetanic potentiation in rats.

High-frequency stimulation eliciting long-term post-tetanic potentiation of neuronal excitation in slices of the rat olfactory cortex was accompanied by changes in the metabolism of phospholipid components of cell membranes. At the first stage of the development of long-term potentiation (10 min after tetanization), there was a reduction in phosphoinositide metabolism. The maintenance phase of the potentiated state (30 min after tetanization) was associated with a three-fold increase in the incorporation of 14C-labeled groups from adenosylmethionine into phosphatidylethanolamine methylation products and with normalization of phosphoinositide metabolism. Sixty minutes after tetanization, when potentiation had decayed, there was activation of phosphoinositide metabolism and the intensity of phosphatidylethanolamine methylation returned to the control level. It is suggested that the phosphoinositide system plays an important role in the induction of long-term potentiation, as well as at the stage of recovery of normal neuronal excitability, while the long-term maintenance phase of elevated neuronal excitability was associated with long-lasting changes in the level of phosphatidylethanolamine methylation. The effect of glutamate receptor agonists on the carbachol-stimulated phosphoinositide response in potentiated slices was found to differ from that in nonpotentiated slices. The development of the long-term potentiated state is thus accompanied by a modulatory action of glutamate on the phosphoinositide response.