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, isoproternol (an agonist of β‐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.