Glucose‐induced electrical activity in rat pancreatic β‐cells: dependence on intracellular chloride concentration

摘要: A rise in glucose concentration depolarizes the β-cell membrane potential leading to electrical activity and insulin release. It is generally believed that closure of KATP channels underlies depolarizing action glucose, though work from several laboratories has indicated existence an additional anionic mechanism. been proposed activates a volume-regulated anion channel, generating inward current due Cl− efflux. This mechanism requires intracellular [Cl−] maintained above its electrochemical equilibrium. hypothesis was tested rat β-cells by varying patch pipette solution using Cl−-permeable antibiotic amphotericin B allow equilibration with cell interior. Under such conditions, depolarization could be evoked 16 mm solutions containing 80 or 150 Cl−. At 40 20 Cl−, subthreshold usually observed, whilst further reduction 12 6 abolished depolarization, some cases glucose-induced hyperpolarization. With gramicidin, which forms Cl−-impermeable pores, induced irrespective solution. latter prevented bumetanide, inhibitor Na+–K+–2Cl− co-transporter. inhibition overcome use high These findings suggest maintenance important determinant support stimulation involves activation channel generation current.