Norepinephrine and cyclic adenosine 3':5'-cyclic monophosphate enhance a nifedipine-sensitive calcium current in cultured rat astrocytes.

We employed two microelectrode current-clamp and voltage-clamp methods to examine the modulation of Ca++ channels by norepinephrine and cyclic AMP (cAMP) in cultured astrocytes from the rat cerebral cortex. Currents owing to Ca++ 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 beta-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++, Cd++, and nifedipine. DbcAMP, or isoproterenol, enhanced the Ba++ current. Modulation of Ca++ channel function in glial cells could have functional implications.