Open AccessFurosemide-Sensitive Calcium Rise Induced by GABAA-Receptor Stimulation in Cultures of Embryonic Rat Striatal Neurons.
Author(s) -
Yuri Ikeda,
Nobuyoshi Nishiyama,
Hiroshi Saito,
Hiroshi Katsuki
Publication year - 1997
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.74.165
Subject(s) - bicuculline , gabaa receptor , muscimol , chemistry , depolarization , extracellular , stimulation , biophysics , striatum , medicine , endocrinology , receptor , biology , biochemistry , dopamine
Changes in [Ca2+]i induced by gamma-aminobutyric acid (GABA) were investigated in primary cultured neurons obtained from fetal rat striatum. GABA and muscimol induced [Ca2+]i rise, and bicuculline blocked the effect of GABA. The [Ca2+]i elevating effect of GABA was also abolished by removal of extracellular Ca2+ or by application of nicardipine. Furthermore, furosemide, an inhibitor of Na+/K+/ 2Cl- co-transport, reversibly inhibited the GABA-induced [Ca2+]i rise. These results suggest that due to the elevated level of intracellular Cl- maintained by Na+/K+/2Cl- transport activity in these neurons, opening of GABAA-receptor-associated Cl- channels results in Cl- efflux, leading to membrane depolarization and activation of L-type voltage-dependent Ca2+ channels.