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Forskolin Stimulation of Cyclic AMP Accumulation in Rat Brain Cortex Slices Is Markedly Enhanced by Endogenous Adenosine

Abstract: Stimulation of cyclic AMP (cAMP) accumulation in rat cortex slices by 1 μM forskolin (F) was markedly reduced (96%) by treatment with adenosine deaminase (ADA). The effect of ADA was progressively less at higher concentrations of F, but still inhibited the response by 50% at 100 μM F. ADA‐mediated inhibition of the cAMP response to 1 μM F was completely reversed by 5 μM 2‐chloroadenosine (CA), an ADA‐resistant analogue. Stimulation by F (controls) and F plus CA (ADA treated) in cortex slices was significantly inhibited by 200 μM caffeine (CAF) and by 10 μM 8‐phenyltheophylline. cAMP accumulation in ADA‐treated cortex slices stimulated with CA at concentrations from 5 to 100 μM was markedly enhanced by 1 μM F. Neither ADA treatment nor 200 μM CAF significantly affected cAMP accumulation in slices stimulated by 1 μM vasoactive intestinal polypeptide or adenylate cyclase in membranes stimulated by 1 μM F. CAF (1 mM) did not significantly increase basal cAMP levels in cortex slices, whereas 1 mM 3‐isobutyl‐1‐methylxanthine caused a significant 80% increase and 100 μM rolipram enhanced cAMP levels by 4.5‐fold. F‐stimulated cAMP accumulation (1 μM) in cortex slices was inhibited 98% by 1 mM CAF and 49% by 1 mM 3‐isobutyl‐1‐methylxanthine, and was enhanced 2.5‐fold by 100 μM rolipram. These data have been interpreted to indicate that the stimulation of cAMP accumulation in rat cortex slices by 1 μM F is predominantly due to synergistic interaction with endogenous adenosine and that the inhibition of this response by CAF is largely due to blockade of adenosine receptors.