Abstract
Insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF) act within the brain to enhance neuronal survival and plasticity. We extend these findings by showing that the presence of both neurotrophins is required to depress the rise in intracellular Ca2+ caused by glutamate in primary cultures of cerebrocortical neurons. IGF-I enhanced expression of BDNF receptors (Trk-B) and increased the ability of BDNF to induce ERK1/2 phosphorylation. This IGF-I-induced increase in BDNF responsiveness describes a new interaction between these peptides in the brain.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Blotting, Western
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Brain-Derived Neurotrophic Factor / metabolism*
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Calcium / metabolism
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Cerebral Cortex / metabolism*
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Glutamic Acid / metabolism
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Insulin-Like Growth Factor I / metabolism*
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Intracellular Fluid / metabolism
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Mice
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Mice, Inbred BALB C
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Neurons / metabolism*
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Phosphorylation
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Receptor, trkB / metabolism
Substances
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Brain-Derived Neurotrophic Factor
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Glutamic Acid
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Insulin-Like Growth Factor I
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Receptor, trkB
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Extracellular Signal-Regulated MAP Kinases
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Calcium