Abstract

SummaryThe cyclic AMP phosphodiesterase (PDE) activity markedly increased in morphologically “differentiated” mouse neuroblastoma cells induced by dibutyryl cyclic AMP, prostaglandin E1 (stimulator of adenylate cyclase) and 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (RO 20-1724, an inhibitor of PDE). Initially, RO 20-1724 decreased the PDE activity by about 50% of control, but later it increased the PDE activity. All of the above agents are known to increase the endogenous level of cyclic AMP, and therefore, in the differentiated cells, a high level of PDE correlated well with a high level of cyclic AMP. X-Irradiation which causes morphological “differentiation” similar to that by dibutyryl cyclic AMP did not increase the PDE activity. Sodium butyrate, 3′,5′-cyclic AMP, 5′-AMP and theophylline which inhibit cell division without causing morphological differentiation did not affect significantly the basal level of PDE. Cycloheximide markedly reduced the PDE activity, whereas actinomycin D did not. A wo...

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