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ATP‐Sensitive Potassium Channel Regulates Astrocytic Gap Junction Permeability by a Ca 2+ ‐Independent Mechanism
Author(s) -
Velasco Ana,
Tabernero Arantxa,
Granda Begoña,
Medina José M.
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.741249.x
Subject(s) - pinacidil , gap junction , tolbutamide , diazoxide , biophysics , potassium channel , chemistry , atp sensitive potassium channel , inward rectifier potassium ion channel , arachidonic acid , intracellular , inhibitory postsynaptic potential , permeability (electromagnetism) , glibenclamide , microbiology and biotechnology , biochemistry , biology , ion channel , membrane , endocrinology , enzyme , insulin , receptor , diabetes mellitus
Using the scrape‐loading technique in cultured astrocytes, we show that sulfonylureas such as tolbutamide and glybenzcyclamide, which inhibit the ATP‐sensitive K+ channel, prevent the inhibition of gap junction permeability caused by several structurally unrelated uncouplers such as oleic acid, arachidonic acid, endothelin‐1, octanol, and α‐glycyrrhetinic acid. When the intracellular level of Ca 2+ was diminished, all the uncouplers tested were still able to inhibit gap junction communication, indicating that their inhibitory effect was not mediated by Ca 2+ . In addition, tolbutamide and glybenzcyclamide prevented the inhibitory effect of these uncouplers in Ca 2+ ‐depleted astrocytes, suggesting that the inhibition of the ATP‐sensitive K+ channel increases gap junction permeability through a Ca 2+ ‐independent mechanism. The activation of the ATP‐sensitive K+ channel caused by potassium channel openers such as diazoxide and pinacidil led to the inhibition of gap junction communication and overcame the effect of sulfonylureas. These results suggest that the ATP‐sensitive K+ channel regulates gap junctional permeability.