Molecular and Morphological Correlates Following Neuronal Deafferentation: A Cortico-Striatal Model

  • G. M. Pasinetti
  • H. W. Cheng
  • J. F. Reinhard
  • C. E. Finch
  • T. H. McNeill
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 296)

Abstract

The ability of neurons to remodel the extent and configuration of their axons and dendrites plays an important role in maintaining function in the central nervous system in normal aging (Cotman and Anderson, 1983; Coleman and Flood, 1987). Conversely, the lack of an appropriate compensatory response of surviving cells to phenomena in the aged brain such as spontaneous neuron loss, deafferentation, or neurotransmitter deficits, is hypothesized to represent a common pathophysiological process in age-related neurodegenerative disorders (Coleman and Flood, 1986). Although the mechanisms governing synaptic remodelling in the adult brain are unknown, we hypothesize that it involves altered genomic expression in surviving neurons of afferent projection systems, whose terminals are induced to sprout and reinnervate deafferentated tissue (Cotman and Nieto-Sampedro, 1984). Moreover, since astrocytes participate in the process of removing degenerating axons and dendrites following a deafferentation lesion (Gage et al., 1988), alterations in the genomic response of these cells could be a critical factor leading to incomplete or delayed reorganization of new synaptic circuits (Scheff et al., 1989).

Keywords

Tyrosine Glucocorticoid Prep Corticosterone eDNA 

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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • G. M. Pasinetti
    • 1
  • H. W. Cheng
    • 1
  • J. F. Reinhard
    • 2
  • C. E. Finch
    • 1
  • T. H. McNeill
    • 1
  1. 1.Andrus Gerontology CenterUniversity of Southern CaliforniaLos AngelesUSA
  2. 2.The Wellcome Research LaboratoriesResearch Triangle ParkUSA

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