We employed two microelectrode current-clamp and voltage-clamp methods to examine the modulation of C a + + channels by norepinephrine and cyclic AMP (CAMP) in cultured astrocytes from the rat cerebral cortex. Currents owing to Cat+ channels were maximized by replacing Ca++ with Ba+ + in the extracellular solution and pharmacologically blocking K + and Na+ currents. In current-clamp experiments, we observed that norepinephrine, isoproterenol (an agonist of @receptors for norepinephrine), or dibutyryl CAMP (dbcAMP, a membrane permeant analogue of CAMP) induced or enhanced slow Ba + +-dependent action potentials in the cells. In voltage-clamp experiments, we confirmed that the slow action potentials were generated by a voltage-activated and Ba++-dependent inward current. This current was mediated by channels that resembled L-type calcium channels (cf. McCleskey et al., Journal of Experimental Biology 124:177-190, 1986) in their voltage-activation range, slow inactivation, and sensitivity to blockage by Co++, C d f + , and nifedipine. DbcAMP, or isoproterenol, enhanced the B a t + current. Modulation of Ca + + channel function in glial cells could have functional implications.