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NO/cGMP/PKG signaling pathway induces magnesium release mediated by mitoK ATP channel opening in rat hippocampal neurons
Author(s) -
Yamanaka Ryu,
Shindo Yutaka,
Hotta Kohji,
Suzuki Koji,
Oka Kotaro
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.06.049
Subject(s) - diazoxide , intracellular , microbiology and biotechnology , depolarization , chemistry , mitochondrion , signal transduction , protein kinase c , biophysics , biology , endocrinology , insulin
Intracellular Mg 2+ concentration ([ Mg 2 + ] i) and NO regulate cell survival and death. To reveal the involvement of NO in intracellular Mg 2+ regulation, we visualized intracellular Mg 2+ using the fluorescent Mg 2+ indicator KMG‐104‐AM in rat hippocampal neurons. Pharmacological experiments using SNAP, 8‐Br‐cGMP, diazoxide and several inhibitors revealed that the NO/cGMP/Protein kinsase G (PKG) signaling pathway triggers an increase in[ Mg 2 + ] i, and that Mg 2+ mobilization is due to Mg 2+ release from mitochondria induced by mitoK ATP channel opening. In addition, Mg 2+ release is potentiated by the positive feedback loop including mitoK ATP channel opening, mitochondrial depolarization and PKC activation.