Cited by 36Neurogenesis and neuroplasticity mechanismsGrowth Hormone and Insulin-like Growth FactorsHypothalamic control of reproductive hormones

Adult-onset deficiency in growth hormone and insulin-like growth factor-I alters oligodendrocyte turnover in the corpus callosum

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Hua, Kun, Forbes, M. Elizabeth, Lichtenwalner, Robin J., Sonntag, William E., Riddle, David R.·2009·Glia

Abstract

Growth hormone (GH) and insulin‐like growth factor‐I (IGF‐I) provide trophic support during development and also appear to influence cell structure, function and replacement in the adult brain. Recent studies demonstrated effects of the GH/IGF‐I axis on adult neurogenesis, but it is unclear whether the GH/IGF‐I axis influences glial turnover in the normal adult brain. In the current study, we used a selective model of adult‐onset GH and IGF‐I deficiency to evaluate the role of GH and IGF‐I in regulating glial proliferation and survival in the adult corpus callosum. GH/IGF‐I‐deficient dwarf rats of the Lewis strain were made GH/IGF‐I replete via twice daily injections of GH starting at postnatal day 28 (P28), approximately the age at which GH pulse amplitude increases in developing rodents. GH/IGF‐I deficiency was initiated in adulthood by removing animals from GH treatment. Quantitative analyses revealed that adult‐onset GH/IGF‐I deficiency decreased cell proliferation in the white matter and decreased the survival of newborn oligodendrocytes. These findings are consistent with the hypothesis that aging‐related changes in the GH/IGF‐I axis produce deficits in ongoing turnover of oligodendrocytes, which may contribute to aging‐related cognitive changes and deficits in remyelination after injury. © 2008 Wiley‐Liss, Inc.

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  1. Paxinos G Watson C The Rat Brain in Stereotaxic Coordinates 1998 4th ed. San Diego, CA Academic Press

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Authors
Hua, K., Forbes, M. E., Lichtenwalner, R. J., Sonntag, W. E., & Riddle, D. R.
Affiliations
  • Wake Forest University Health Sciences (US)
  • University of Oklahoma Health Sciences Center (US)
Corresponding author
Riddle, David R.
Venue
Glia
Publisher
Wiley
Published
2008-12-29
Volume
57
Issue
10
Pages
1062-1071
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
OpenAlex
W2036293292
Cited by
36
References
94
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 4 · 2017: 1 · 2016: 1 · 2015: 2 · 2013: 4 · 2012: 6
FWCI
0.61
Type
journal article
Language
en
Open access
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01ag026607-06)
  • National Institute on Aging (#R01AG026607, P01AG11370, P01AG011370)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
growth hormone deficiency, insulin-like growth factor I, corpus callosum, glial cell proliferation, oligodendrocyte survival, white matter, aging, remyelination, somatotropic axis
MeSH terms
Aging, Animals, Cell Survival, Cognition Disorders, Corpus Callosum, Disease Models, Animal, Female, Insulin-Like Growth Factor I, Male, Memory Disorders, Myelin Sheath, Nerve Fibers, Myelinated, Nerve Regeneration, Oligodendroglia, Growth Hormone, Substance Withdrawal Syndrome, Cell Proliferation, Rats

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