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(The FASEB Journal. 2006;20:A536)
© 2006 FASEB
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357.5

A Study of Insulin-like Growth Factor-I Receptor Immunoreactivity in the Supraoptic Nucleus of Young and Old Female B6D2F1 Mice

Farzin Yaghmaie1, Omar Saeed2, Steven A. Garan3, Arvin M. Gouw4, Tien Tran4, Jacqueline Ho4, Liu Y. Zhao4, Mark A. Voelker5 and Paola S. Timiras4

1 Medical College of Virginia, 507A St. James St., Richmond, VA, 23220,
2 New York Medical College, 1403 Old Farm Rd, Valhalla, NY, 10595,
3 Aging Research Centre, 145 Columbia St. West, Waterloo, Ontario, N2L5C9, Canada,
4 Molecular & Cell Biology, University of California, Berkeley, 237 Hildebrand Hall, Berkeley, CA, 94720,
5 BioTime, Inc., 6121 Hollis Street, Emeryville, CA, 94608

ABSTRACT

Insulin-like Growth Factor-I (IGF-I) is a critical hormone that regulates both development and aging with its fluctuating expression throughout the lifespan. Multiple studies have demonstrated that IGF-I levels in the mammalian brain decline with age. However, without simultaneously tracking tissue sensitivity to IGF-I, its net biological effect remains undefined. Taking IGF-I receptor (IGF-IRc) immunoreactivity as a measure of tissue sensitivity, our study measures its levels in the supraoptic nucleus (SON) of the hypothalamus. With its central location, the SON is the major arbiter of posterior pituitary activity, and IGF-I action in the SON specifically influences vasopressin release, and provides neuroprotection. Current results from SON in ad libitum fed mice show a significant reduction in percentage of IGF-IRc-positive cells from 44% in young (5 week old) to 36% in old (22 month old). This reduced sensitivity of SON IGF-I with age, parallels the declining IGF-I levels in other brain areas and implies that the overall biological action of IGF-I on the aging phenotype is reduced. Whether this reduction is an adaptive response to the aging process or a causative factor resulting in the aged phenotype remains to be established.

Supported by NIH AG 19145-04 and BioTime, Inc., Emeryville, CA.





This Article
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Right arrow Articles by Timiras, P. S.