Abstract
Cultured embryonic cortical neurons from rats were used to explore mechanisms of activity-dependent neuronal survival. Cell survival was increased by the activation of voltage-sensitive calcium channels (VSCCs) but not by activation of N-methyl-D-aspartate receptors. These effects correlated with the expression of brain-derived neurotrophic factor (BDNF) induced by these two classes of calcium channels. Antibodies to BDNF (which block intracellular signaling by BDNF, but not by nerve growth factor, NT3, or NT4/5) reduced the survival of cortical neurons and reversed the VSCC-mediated increase in survival. Thus, endogenous BDNF is a trophic factor for cortical neurons whose expression is VSCC-regulated and that functions in the VSCC-dependent survival of these neurons.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antibodies
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Brain-Derived Neurotrophic Factor
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Calcium Channels / physiology*
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Cell Division / drug effects
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Cell Survival / drug effects
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Cells, Cultured
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Cerebral Cortex / cytology*
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Cyclic AMP Response Element-Binding Protein / metabolism
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Embryo, Mammalian
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Glutamates / pharmacology
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Glutamic Acid
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N-Methylaspartate / pharmacology
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Nerve Growth Factors / biosynthesis
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Nerve Growth Factors / genetics
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Nerve Growth Factors / immunology
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Nerve Growth Factors / physiology*
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Nerve Tissue Proteins / biosynthesis
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / immunology
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Nerve Tissue Proteins / physiology*
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Neurons / cytology*
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Phosphorylation
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Potassium Chloride / pharmacology
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Rats
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Receptors, N-Methyl-D-Aspartate / physiology
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Signal Transduction
Substances
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Antibodies
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Brain-Derived Neurotrophic Factor
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Calcium Channels
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Cyclic AMP Response Element-Binding Protein
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Glutamates
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Nerve Growth Factors
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Nerve Tissue Proteins
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Receptors, N-Methyl-D-Aspartate
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Glutamic Acid
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N-Methylaspartate
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Potassium Chloride