PARTICIPATION OF ADENOSINE RECEPTORS IN ANTIFEIN-MEDIATED REGULATION OF NEURONAL CHROMATIN

The mechanisms of regulation of transcriptional activity of chromatin were studied. Ethylnorantifein (a memory enhancer) and its analogs wer e used to study the metabolic links (adenylate cyclase and calcium and phospholipid-dependent protein kinase) of signal transduction from ad enosine receptors. Rat striatum and cerebral cortex preparations were used to model the biochemical conditions for the functioning of A(1) a nd A(2) adenosine receptors. In contrast to adenosine deaminase-resist ant derivatives of adenosine (PIA(3), NECA, and isobutyl methylxanthin e) antifeins produced no effect on adenylate cyclase mediated by adeno sine receptors. Antifeins (10(-7) and 10(-3) M) did not directly affec t the membrane pool of protein kinase C. The data argue against explai ning the effects produced by antifeins on the functions of chromatin a s a triggering of membrane acceptor systems. Increasing activity of pr otein kinase C after 180 min revealed in this study was probably due t o the effects of ethymizol and its demethylated derivatives, which inc rease the synthesis of RNA and synaptosomal proteins. Direct regulatio n of the functions of cerebral cell chromatin by neuroactive compounds is discussed.