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

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...

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Veröffentlicht in:The FASEB journal 2006-03, Vol.20 (4), p.A536-A536
Hauptverfasser: Yaghmaie, Farzin, Saeed, Omar, Garan, Steven A., Gouw, Arvin M., Tran, Tien, Ho, Jacqueline, Zhao, Liu Y., Voelker, Mark A., Timiras, Paola S.
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Sprache:eng
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Zusammenfassung: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.
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.20.4.A536