Using primary neuronal or astrocyte cultures from the striatum of the embryonic mouse, we have observed that the β-adrenergic agonist isoprenaline (10−5 M) induced a more pronounced accumulation of cAMP in astrocytes than in neurons. In both cell types, the α-adrenergic selective agonist methoxamine (10−4 M), which alone did not affect the production of cAMP, potentiated the isoprenaline-evoked response. In support of these observations, when associated α2-noradrenergic and D1-dopaminergic responses were prevented, the mixed α1- and β-adrenergic agonist noradrenaline (10−5 M) induced a production of cAMP which was totally blocked by propranolol (10−6 M) and partially abolished by prazosin (10−6 M). Since experiments were made in the presence of 3-isobutyl-1-methylxanthine (1 mM), the observed effects on cAMP accumulation were not related to a modulation of phosphodiesterase activities. In addition, both in astrocytes and in neurons, the potentiation by α1-adrenergic agonists of the β-adrenergic-evoked response required external calcium. Using INDO 1 as a fluorescent probe, methoxamine (25 μM) was shown to induce in astrocytes an increase in cytosolic calcium concentration which was prolonged by isoprenaline (10−5 M) only in the presence of external calcium. These results suggest that the prolonged increase in cytosolic calcium concentration linked to the activation of α1- and β-adrenergic receptors is responsible for the potentiation of the β-adrenergic-induced production of cAMP, which is partially dependent on external calcium.