Glutamate mobilizes [Zn2+]i through Ca2+-dependent reactive oxygen species accumulation

摘要: Liberation of zinc from intracellular stores contributes to oxidant-induced neuronal injury. However, little is known regarding how endogenous oxidant systems regulate free ([Zn2+]i). Here we simultaneously imaged [Ca2+]i and [Zn2+]i study acute changes in cultured rat forebrain neurons after glutamate receptor activation. Neurons were loaded with fura-2FF FluoZin-3 follow [Zn2+]i, respectively. treated (100 μM) for ten minutes gave large Ca2+ responses that did not recover termination the stimulus. Glutamate also increased however glutamate-induced completely dependent on entry, appeared arise entirely internal stores, substantially reduced by co-application membrane-permeant chelator TPEN during treatment. Pharmacological maneuvers revealed a number producing systems, including nitric oxide synthase, phospholipase A2, mitochondria all contributed changes. We found no evidence buffered conclude transients are caused part -induced reactive oxygen species arises both cytosolic mitochondrial sources.