Effects of 4-aminopyridine and tetraethylammonium on the depolarization by GABA of cultured satellite glial cells.
4-Aminopyridine (4-AP) which selectively blocks K+-conductance of excitable membranes, reversibly abolished the depolarization by gamma-aminobutyric acid (GABA) of cultured satellite glial (SG) cells, but did not or only slightly affect the action of GABA on dorsal root ganglion (DRG) neurons. It is therefore suggested that the depolarization of glial cells by GABA is an indirect effect due to the accumulation of K+ which is released from adjacent neurons during their depolarization by the amino acid. Tetraethylammonium (TEA) had no effect on the GABA depolarization at a concentration of 15 mM but produced a slight reduction at higher concentrations (60--70 mM).
D000631:Aminopyridines / Q000494:pharmacology*; D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism; D018756:GABA Antagonists; D008564:Membrane Potentials / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D051381:Rats; D013757:Tetraethylammonium Compounds / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D000631:Aminopyridines; D002712:Chlorides; D018756:GABA Antagonists; D013757:Tetraethylammonium Compounds; D005680:gamma-Aminobutyric Acid; D011188:Potassium