Changes in mitochondrial NAD(P)H and glutamate-induced delayed calcium deregulation in cultured rat cerebellar granule neurons |
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| Authors: | A M Surin S N Zobova G R Tukhbatova Y E Senilova V G Pinelis B I Khodorov |
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| Institution: | (1) Department of Zoology, Center for Neurosciences and Cellular Biology, University of Coimbra, 3004-517 Coimbra, Portugal;(2) Department of Anatomy, Microbiology and Pathology, University of Minnesota Medical School, Duluth, USA;(3) Department of Biochemistry, Center for Neurosciences and Cellular Biology, Medical School, University of Coimbra, Coimbra, Portugal;(4) Department of Biochemistry and Molecular Biology, University of Minnesota Medical School, Duluth, USA |
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| Abstract: | Changes in cytosolic Ca2+]i, mitochondrial potential (ΔVm), and mitochondrial NAD(P)H autofluorescence were compared in experiments on cultured cerebellar
granule cells co-loaded with Ca2+ indicator Fluo-3FF or mitochondrial potential-sensitive probe Rh123. In the majority of neurons (94% of cells, n = 205, 28 experiments) the delayed Ca2+ deregulation (DCD) induced by Glu (100 μM) was preceded by more or less prolonged decrease in NAD(P)H, which in 57% of cells
underwent a further (secondary) reduction during DCD development. To clarify the origin of these changes in NAD(P)H production
during DCD we examined the effects of the protonophore FCCP on NAD(P)H increase induced by the electron chain blocker CN (3
mM) application. The data suggest that a pronounced lowering of mitochondrial pH during DCD contributed to the mechanism of
Glu-induced suppression of NAD(P)H production. |
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