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).
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© 1991 Plenum Press, New York
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Pasinetti, G.M., Cheng, H.W., Reinhard, J.F., Finch, C.E., McNeill, T.H. (1991). Molecular and Morphological Correlates Following Neuronal Deafferentation: A Cortico-Striatal Model. In: Timiras, P.S., Privat, A., Giacobini, E., Lauder, J., Vernadakis, A. (eds) Plasticity and Regeneration of the Nervous System. Advances in Experimental Medicine and Biology, vol 296. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8047-4_23
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DOI: https://doi.org/10.1007/978-1-4684-8047-4_23
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