Dendritic stability in a model of adult-onset IGF-I deficiency

Growth Horm IGF Res. 2005 Oct;15(5):337-48. doi: 10.1016/j.ghir.2005.07.002.

Abstract

Objective: A significant decrease in plasma levels of insulin-like growth factor-I (IGF-I) is one of the most robust hallmarks of aging and may contribute to functional changes associated with senescence. This study examined the role of IGF-I in the maintenance of adult dendritic morphology.

Design: We utilized a model of the aging-related decrease in plasma IGF-I to examine whether such a decrease, in itself, leads to dendritic changes in the cerebral cortex. The dw/dw rat, originally of the Lewis strain, suffers from a spontaneous mutation in which growth hormone (GH) production is severely decreased. Since GH is responsible for the production of circulating IGF-I by the liver, these animals are deficient in plasma IGF-I. Homozygous dw/dw rats were administered porcine GH to sustain IGF-I levels during development and then GH injections were stopped as adults in order to examine the effects of adult-onset GH and IGF-I deficiency. Animals sacrificed after two or eight weeks of GH and IGF-I deficiency were compared to age-matched dw/dw animals that received GH both developmentally and throughout adulthood (GH/IGF-I replete). The dendritic arbors of pyramidal neurons in cingulate cortex were labeled by intracellular injection and reconstructed in three dimensions.

Results: Comparing GH/IGF-I replete and deficient dw/dw rats, we found no differences in the apical or basal arbors of either layer two or layer five pyramidal neurons.

Conclusions: These findings indicate that a decrease in plasma levels of IGF-I is not sufficient in itself to produce dendritic changes like those seen in aging animals.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aging / physiology
  • Animals
  • Body Weight / drug effects
  • Cerebral Cortex / pathology
  • Dendrites / pathology*
  • Female
  • Growth Hormone / deficiency
  • Growth Hormone / pharmacology
  • Homozygote
  • Insulin-Like Growth Factor I / deficiency*
  • Male
  • Rats
  • Rats, Mutant Strains

Substances

  • Insulin-Like Growth Factor I
  • Growth Hormone