Magnesium blocks the loss of protein kinase C, leads to a transient translocation of PKCα and PKCε, and improves recovery after anoxia in rat hippocampal slices

Molecular Brain Research

Volumn 136, Issue 1-2, 2005, Pages 104-111

  Libien, Jenny ^a   Sacktor, Todd Charlton ^a   Kass, Ira S ^a  

^a SUNY DOWNSTATE MEDICAL CENTER   (United States)

Author keywords

Anoxia; Hippocampus; Hypoxia; Ischemia; Magnesium; Protein kinase C

Indexed keywords

ISOENZYME; MAGNESIUM; PROTEIN KINASE C; PROTEIN KINASE C ALPHA; PROTEIN KINASE C BETA1; PROTEIN KINASE C BETA2; PROTEIN KINASE C EPSILON; PROTEIN KINASE C GAMMA; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL TISSUE; ARTICLE; BRAIN HYPOXIA; BRAIN INJURY; BRAIN SLICE; CONTROLLED STUDY; CORRELATION ANALYSIS; DISEASE MODEL; DOWN REGULATION; DRUG MECHANISM; DRUG RESPONSE; HIPPOCAMPUS; MEMBRANE; NEUROPROTECTION; NONHUMAN; PRIORITY JOURNAL; PROTEIN LOCALIZATION; RAT; REOXYGENATION; SYNAPSE; SYNAPTIC TRANSMISSION; TIME;

ANIMALS; ANOXIA; BLOTTING, WESTERN; ELECTROCARDIOGRAPHY; HIPPOCAMPUS; MAGNESIUM; MEMBRANE POTENTIALS; PROTEIN KINASE C; PROTEIN KINASE C-ALPHA; PROTEIN KINASE C-EPSILON; PROTEIN TRANSPORT; RATS; RATS, SPRAGUE-DAWLEY; SUBCELLULAR FRACTIONS; TIME FACTORS;

EID: 18944373592     PISSN: 0169328X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.molbrainres.2005.01.005     Document Type: Article

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