Journal
FRONTIERS IN NEUROENDOCRINOLOGY
Volume 27, Issue 4, Pages 391-403Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2006.09.001
Keywords
akt; beta-catenin; glia; glycogen synthase kinase 3; mitogen-activated protein kinase; neuronal development; neuroprotection; phosphatidyloinositol 3-kinase; synaptic plasticity; tau
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Accumulating evidence suggests that insulin-like growth factor-I (IGF-I) and estradiol interact to regulate neural function. In this review, we focus on the cellular and molecular mechanisms involved in this interaction. The expression of estrogen receptors (ERs) and IGF-I receptor is cross-regulated in the central nervous system and many neurons and astrocytes coexpress both receptors. Furthermore, estradiol activates IGF-I receptor and its intracellular signaling. This effect may involve classical ERs since recent findings suggest that ER alpha may affect IGF-I actions in the brain by a direct interaction with some of the components of IGF-I signaling. In turn, IGF-I may regulate ER transcriptional activity in neuronal cells. In conclusion, ERs appear to be part of the signaling mechanism of IGF-I, and IGF-I receptor part of the mechanism of estradiol signaling in the nervous system. (c) 2006 Elsevier Inc. All rights reserved.
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