ALPHA-ADRENERGIC RECEPTOR MODULATION OF BETA-ADRENERGIC, ADENOSINE AND PROSTAGLANDIN-E1 INCREASED ADENOSINE 3'-5'-CYCLIC MONOPHOSPHATE LEVELS IN PRIMARY CULTURES OF GLIA

Abstract

.beta.-Adrenergic agonists, adenosine and prostaglandin E1 increased the level of c[cyclic]AMP in glial cultures prepared from rat cerebral cortical tissue. Cholera toxin also increased cAMP levels in these cultures. The accumulation of cAMP in response to each of these agents, including cholera toxin, was partially blocked (50-80%) by simultaneous .alpha.-adrenergic receptor stimulation. Basal levels of cAMP were not affected by .alpha.-adrenergic agonists. In glia, .alpha.-adrenergic receptors may serve to modulate the level of cAMP which normally accumulates in response to a number of neurohumoral substances. The modulatory effect of .alpha.-adrenergic agents does not appear to reduce cAMP accumulation by activating phosphodiesterase since the effect was not blocked by a potent inhibitor of this enzyme. The modulatory effect of .alpha.-adrenergic receptor activation may result from an interaction which takes place at some point in between adenylate cyclase-associated-membrane receptors and the enzymatic degradation of cAMP.