{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T18:06:03Z","timestamp":1773425163791,"version":"3.50.1"},"reference-count":40,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,9,28]],"date-time":"2005-09-28T00:00:00Z","timestamp":1127865600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:p>A rise in glucose concentration depolarizes the \u03b2\u2010cell membrane potential leading to electrical activity and insulin release. It is generally believed that closure of K<jats:sub>ATP<\/jats:sub> channels underlies the depolarizing action of glucose, though work from several laboratories has indicated the existence of an additional anionic mechanism. It has been proposed that glucose activates a volume\u2010regulated anion channel, generating an inward current due to Cl<jats:sup>\u2212<\/jats:sup> efflux. This mechanism requires that intracellular [Cl<jats:sup>\u2212<\/jats:sup>] is maintained above its electrochemical equilibrium. This hypothesis was tested in rat \u03b2\u2010cells by varying [Cl<jats:sup>\u2212<\/jats:sup>] in the patch pipette solution using the Cl<jats:sup>\u2212<\/jats:sup>\u2010permeable antibiotic amphotericin B to allow Cl<jats:sup>\u2212<\/jats:sup> equilibration with the cell interior. Under such conditions, a depolarization and electrical activity could be evoked by 16 m<jats:sc>m<\/jats:sc> glucose with pipette solutions containing 80 or 150 m<jats:sc>m<\/jats:sc> Cl<jats:sup>\u2212<\/jats:sup>. At 40 or 20 m<jats:sc>m<\/jats:sc> Cl<jats:sup>\u2212<\/jats:sup>, a subthreshold depolarization was usually observed, whilst further reduction to 12 or 6 m<jats:sc>m<\/jats:sc> abolished depolarization, in some cases leading to a glucose\u2010induced hyperpolarization. With a pipette solution containing gramicidin, which forms Cl<jats:sup>\u2212<\/jats:sup>\u2010impermeable pores, glucose induced a depolarization and electrical activity irrespective of [Cl<jats:sup>\u2212<\/jats:sup>] in the pipette solution. Under the latter conditions, glucose\u2010induced electrical activity was prevented by bumetanide, an inhibitor of the Na<jats:sup>+<\/jats:sup>\u2013K<jats:sup>+<\/jats:sup>\u20132Cl<jats:sup>\u2212<\/jats:sup> co\u2010transporter. This inhibition could be overcome by the use of amphotericin B with a high [Cl<jats:sup>\u2212<\/jats:sup>] pipette solution. These findings suggest that the maintenance of high intracellular [Cl<jats:sup>\u2212<\/jats:sup>] in the \u03b2\u2010cell is an important determinant in glucose\u2010induced depolarization, and support the hypothesis that \u03b2\u2010cell stimulation by glucose involves activation of the volume\u2010regulated anion channel and generation of an inward Cl<jats:sup>\u2212<\/jats:sup> current.<\/jats:p>","DOI":"10.1113\/jphysiol.2005.093740","type":"journal-article","created":{"date-parts":[[2005,7,15]],"date-time":"2005-07-15T00:13:42Z","timestamp":1121386422000},"page":"137-144","source":"Crossref","is-referenced-by-count":63,"title":["Glucose\u2010induced electrical activity in rat pancreatic \u03b2\u2010cells: dependence on intracellular chloride 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