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The K‐ATP channel regulates the effect of Ca 2+ on gap junction permeability in cultured astrocytes
Author(s) -
Granda Begoña,
Tabernero Arantxa,
Sánchez-Abarca Luis Ignacio,
Medina José M
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00390-1
Subject(s) - tolbutamide , gap junction , permeability (electromagnetism) , biophysics , chemistry , depolarization , intracellular , channel blocker , membrane channel , membrane , calcium , biochemistry , endocrinology , biology , insulin , organic chemistry
Using the scrape‐loading technique we show that tolbutamide and glybenzcyclamide, two inhibitors of the K + channel sensitive to ATP (K‐ATP channel), partially prevent the inhibition of gap junction permeability promoted by Ca 2+ in cultured astrocytes. This effect was dose‐dependent, reaching a maximum at 400 μM and 1 μM of tolbutamide and glybenzcyclamide, respectively. The presence of the Ca 2+ ionophore A‐23187 strongly reduced the concentration of Ca 2+ required to block gap junction permeability but did not abolish the effect of tolbutamide and glybenzcyclamide. These results suggest that the effect of these two compounds are not brought about by control of the intracellular concentration of Ca 2+ but probably by the promotion of plasma membrane depolarization.