The regulatory pathways of chromatin transcription in neurons have been studied. The metabolic events (adenylate cyclase, Ca/phospholipid-dependent protein kinase C) involved in signal transduction via adenosine receptors were investigated with the application of pharmacological tools--the memory stimulant ethylnorantifeine and its structural analogs. It has been modelled the biochemical condition of A1 and A2 adenosine receptors in the cortex and the striatum of rat brain. The antifeines did not influence AC of A1 or A2 receptors, unlike the non-metabolizing adenosine derivatives -PIA, NECA and isobutylmethylcanthine. No direct effect of antifeines (10(-7)-10(-3) M) on membrane-bound protein kinase C was established. The data obtained failed to provide evidence for the antifeine effect on the functional activity of chromatin with regard to the triggering role of membrane acceptor systems. The possibility of direct control of the chromatin functional activity by neuroactive drugs is discussed.