ADENOSINE-3′,5′-MONOPHOSPHATE (cAMP) has often been suggested as a second messenger which mediates the action of a variety of hormones 1. The presynaptic location of the cAMP system, and the demonstration of a cAMP dependent protein kinase in mammalian brain tissue, suggest a possible role for cAMP in the central nervous system2. It has been suggested, for example, that cAMP may participate in the secretion of acetylcholine3 and the hypophyseal releasing factors in the hypothalamus3. In vitro4 and in vivo5 studies indicate that some putative neurohormones increase cAMP synthesis by activating adenyl cyclase. The effect of cAMP on brain biogenic amines has also been studied. Shein et al.6 showed an increase in serotonin (5-HT) synthesis from tryptophan by cAMP in pineal culture. Tagliamonte et al. 7 reported that injection of cAMP into the lateral ventricle of rats increases the 5-HT turnover in brain. Results obtained in our laboratory in mice (I. K. H., H. H. L. and E. L. W., unpublished results) indicate that cAMP decreases the endogenous level of cerebral norepinephrine (NE) and dopamine (DA) as well as the conversion of 14C-tyrosine into 14C-CA (catecholamines).