Ca2+ Buffering Capacity of Mitochondria After Oxygen-Glucose Deprivation in Hippocampal Neurons
Autor: | Kimio Akagawa, Yasuhide Iwao, Tatsuya Mishima, Kensuke Tanaka, Takehiko Iijima, Kei Suga |
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Rok vydání: | 2008 |
Předmět: |
medicine.medical_specialty
Ischemia Mitochondrion Hippocampal formation Biology Hippocampus Biochemistry Membrane Potentials Cellular and Molecular Neuroscience Internal medicine medicine Animals Rats Wistar Neurons Membrane potential Glutamate receptor General Medicine Hyperpolarization (biology) medicine.disease Mitochondria Rats Oxygen Cytosol Glucose Endocrinology Apoptosis Calcium |
Zdroj: | Neurochemical Research. 34:221-226 |
ISSN: | 1573-6903 0364-3190 |
Popis: | In an earlier study, we showed that mitochondria hyperpolarized after short periods of oxygen-glucose deprivation (OGD), and this response appeared to be associated with subsequent apoptosis or survival. Here, we demonstrated that hyperpolarization following short periods of OGD (30 min; 30OGD group) increased the cytosolic Ca(2+) ([Ca(2+)](c)) buffering capacity in mitochondria. After graded OGD (0 min (control), 30 min, 120 min), rat cultured hippocampal neurons were exposed to glutamate, evoking Ca(2+)influx. The [Ca(2+)](c) level increased sharply, followed by a rapid increase in mitochondrial Ca(2+) [Ca(2+)](m). The increase in the [Ca(2+)](m) level accompanied a reduction in the [Ca(2+)](c) level. After reaching a peak, the [Ca(2+)](c) level decreased more rapidly in the 30OGD group than in the control group. This buffering reaction was pronounced in the 30OGD group, but not in the 120OGD group. The enhanced buffering capacity of the mitochondria may be linked to preconditioning after short-term ischemic episodes. |
Databáze: | OpenAIRE |
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