The possible role of adenosine as a modulator or transmitter in the central nervous system was tested by measuring its effects on LRM55 astroglial cells. Two related cellular responses were measured-receptor activated increases in intracellular CAMP and CAMP-mediated taurine release. Taurine is a neuroinhibitory amino acid that is taken up, stored, and released from primary cultures of astrocytes and astroglial cells. Three-minute incubations of cells with adenosine caused a dosedependent accumulation of intracellular CAMP and release of the taurine @& = 5.0 X M and 1.6 X M, respectively). That the cellular responses were mediated through the activation of spec& adenosine receptors was indicated by the observations that the adenosine receptor antagonist isobutylmethylxanthine (IBMX) but not the beta-adrenergic receptor antagonist 1-propranolol inhibited responses to adenosine. The study of various adenosine analogs showed a rank order of potency (chloroadenosine = 5'-(N-ethyl)carboxamidoadenosine > N6-(L-2-phenyliipropyl)-adenosine > cyclohexyladenosine = cyclopentyladenosine) characteristic of the low affinity A,-type adenosine receptors that have been associated with CAMP elevation in several tissues. These results indicate that, in addition to directly affecting neurons, adenosine may have a primary site of action on astroglial cells resulting in taurine release and subsequent inhibition of neuronal activity.