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1. Insulin-like growth factor-I enhances the biological activity of brain-derived neurotrophic factor on cerebrocortical neurons.

Author

McCusker RH, McCrea K, Zunich S, Dantzer R, Broussard SR, Johnson RW, and Kelley KW

Subjects
Animals, Blotting, Western, Calcium metabolism, Extracellular Signal-Regulated MAP Kinases metabolism, Glutamic Acid metabolism, Intracellular Fluid metabolism, Mice, Mice, Inbred BALB C, Phosphorylation, Receptor, trkB metabolism, Brain-Derived Neurotrophic Factor metabolism, Cerebral Cortex metabolism, Insulin-Like Growth Factor I metabolism, Neurons metabolism
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.

Published
2006
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