Premium
Norepinephrine and cyclic adenosine 3′:5′‐cyclic monophosphate enhance a nifedipine‐sensitive calcium current in cultured rat astrocytes
Author(s) -
MacVicar B. A.,
Tse F. W. Y.
Publication year - 1988
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440010602
Subject(s) - nifedipine , voltage clamp , biophysics , norepinephrine , agonist , cyclic adenosine monophosphate , adenosine , medicine , endocrinology , biology , patch clamp , current clamp , voltage dependent calcium channel , extracellular , calcium channel , calcium , electrophysiology , membrane potential , receptor , neuroscience , biochemistry , dopamine
Abstract 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.