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Previous work reported that 500 nm [Ca2+]i causes the exocytosis of insulin-containing granules [30, 31], while lower concentrations (100�C500 nm) rather promote the docking of insulin-containing granules [32]. In order to determine whether glutamate-induced depolarization and Ca2+ influx was strong enough to evoke insulin release, we used Fura-PE3 ratiometric imaging to assess to what extent glutamate elicited a rise in [Ca2+]i [30, 33]. In the absence of glutamate, the [Ca2+]i was low (60?��?15 nm; n?=?9; N?=?3; Figure?4D). External glutamate (600 ��m) led to an about threefold increase of [Ca2+]i (176?��?13 nm; n?=?8; N?=?3; p was measured using whole-cell patch-clamp in a K+-based ATP-free pipette solution [28, 33, 35]. After establishing the whole-cell configuration, KATP conductance rapidly increased to a peak, usually within 2 min, with a mean maximum of 3.9?��?0.1 nS/pF (n?=?20; N?=?6; Figure?6A). Glutamate treatment reduced the peak amplitude to 3.1?��?0.2 nS/pF (n?=?20; N?=?6; p?