title: Adult-onset deficiency in growth hormone and insulin-like growth factor-I alters oligodendrocyte turnover in the corpus callosum.
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.
authors.affiliation: Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1010, USA.
authors.forename: Kun
authors.initials: K
authors.lastname: Hua
authors.forename: M Elizabeth
authors.initials: ME
authors.lastname: Forbes
authors.forename: Robin J
authors.initials: RJ
authors.lastname: Lichtenwalner
authors.forename: William E
authors.initials: WE
authors.lastname: Sonntag
authors.forename: David R
authors.initials: DR
authors.lastname: Riddle
mesh_terms: D000375:Aging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D049109:Cell Proliferation; D002470:Cell Survival / Q000502:physiology; D003072:Cognition Disorders / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003337:Corpus Callosum / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D013006:Growth Hormone / Q000172:deficiency* / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000172:deficiency*; D008297:Male; D008569:Memory Disorders / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D009186:Myelin Sheath / Q000378:metabolism / Q000473:pathology; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000473:pathology; D009416:Nerve Regeneration / Q000502:physiology; D009836:Oligodendroglia / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone