title: Mechanisms of GABA- and glycine-induced increases of cytosolic Ca2+ concentrations in chick embryo ciliary ganglion cells.
abstract: We used fura-2 microfluorometry and the gramicidin-perforated patch clamp technique in an attempt to clarify the mechanisms underlying the GABA- and glycine-induced increases in the cytosolic Ca2+ concentration ([Ca]in) in acutely isolated chick embryo ciliary ganglion neurons. GABA, glycine, and isoguvacine, but not baclofen, increased [Ca]in in a dose- and a Ca2+-dependent manner. The GABA-induced [Ca]in increase was inhibited by bicuculline and picrotoxin, and potentiated by pentobarbital, flunitrazepam, and alphaxalone, whereas the glycine-induced [Ca]in increase was inhibited by strychnine but not by bicuculline or picrotoxin. L- and N-type Ca2+ channel blockers inhibited the GABA- and glycine-induced [Ca]in increases, whereas Bay K-8644 potentiated these responses. These responses were also substantially potentiated by blockers of various K+ channels and by lowering the external Cl- concentrations. The high KCI- and nicotine-induced [Ca]in increases were substantially reduced during continuous stimulation with either 2 microM GABA or 1 mM glycine. Electrophysiological studies indicated that the reversal potential of the GABA-induced current exhibited a more depolarized value than the resting membrane potential in 17 of the 25 cells examined. Taken together, these results suggest that both GABA and glycine depolarize the membrane potentials by increasing Cl- conductance via respective receptors and thus increase the Ca2+ influxes through L- and N-type voltage-dependent Ca2+ channels.
authors.affiliation: Department of Physiology, Kagoshima University Faculty of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Sorimachi
authors.forename: J S
authors.initials: JS
authors.lastname: Rhee
authors.forename: M
authors.initials: M
authors.lastname: Shimura
authors.forename: N
authors.initials: N
authors.lastname: Akaike
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002642:Chick Embryo; D002712:Chlorides / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism*; D005456:Fluorescent Dyes; D016257:Fura-2; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005726:Ganglia, Parasympathetic / Q000196:embryology* / Q000378:metabolism* / Q000648:ultrastructure; D005998:Glycine / Q000494:pharmacology*; D008345:Manganese / Q000494:pharmacology; D009538:Nicotine / Q000494:pharmacology; D026902:Potassium Channel Blockers; D011189:Potassium Chloride / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D013050:Spectrometry, Fluorescence; D015091:beta-Alanine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
chemical_list: D002712:Chlorides; D005456:Fluorescent Dyes; D018755:GABA Agonists; D018756:GABA Antagonists; D026902:Potassium Channel Blockers; D011963:Receptors, GABA-A; D015091:beta-Alanine; D008345:Manganese; D005680:gamma-Aminobutyric Acid; D011189:Potassium Chloride; D009538:Nicotine; D002118:Calcium; D005998:Glycine; D016257:Fura-2