Molecular and Morphological Correlates Following Neuronal Deafferentation: A Cortico-Striatal Model
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).
KeywordsTyrosine Glucocorticoid Prep Corticosterone eDNA
Unable to display preview. Download preview PDF.
- Buttyan R., Olsson C.A., Pintar J., Chang C., Bandyk M., NG P.Y., and Sawczuk I.S., 1989, Induction of the TRPM-2 gene in cells undergoing programmed cell death. Mol. and Cell. Biol., 9:3473.Google Scholar
- Capetanaki Y.G., Ngai J., and Lazarides E., 1984, Regulation of the expression of genes coding for the intermediate filament subunits vimentin, desmin, and glial fibrillary acidic protein, in: “Molecular Biology of the Cytoskeleton,” Cold Spring Harbor Press.Google Scholar
- Cheng H.W., Anavi Y., Goshgarian H., McNeill T.H., and Rafols J.A., 1988, Loss and recovery of striatal dendritic spines following lesions in the cerebral cortex of adult and aged mice, Soc. Neurosci. Abst., 14:1219.Google Scholar
- Cotman C.W., and Anderson K.J., 1983, Synaptic plasticity and functional stabilization in the hippocampal formation: possible role in Alzheimer disease, in: “Advances in Neurology,” S.G. Waxman, ed., Vol. 47 Functional recovery in Neurological Disease, Raven Press, New York, NY.Google Scholar
- Geddes S.W., Wong J., Choi B.H., Kim R. C., Cotman C.W., and Miller F.D., 1990, Increased expression of embrionyc growth associated mRNA in Alzheimer disease, Neurosci. Lett., (in press).Google Scholar
- Lozano A.M., Doster S.K., Aguayo A.J., and Willard M.B., 1987, Immunoreactivity to GAP-43 in axotomized and regenerating retinal ganglion cells of adult rats, Abstr. Soc. Neurosci., 13:1389.Google Scholar
- May P.C., Lampert-Etchelles M., Johnson S.A., Poirier J., Master J., and Finch C.E., 1990, Dynamics of gene expression for hippocampal glycoprotein elevated in alzheimer’s disease and in response to experimental lesion in rat, Neuron, (in press).Google Scholar
- McNeill T.H., Brown S.A., Rafols J.A., and Shoulsson I., 1989, Atrophy of medium spiny I striatal dendrites in advanced Parkinson’s disease, Brain Res., 455:158.Google Scholar
- McNeill T.H. and Koeck L.L., 1990, Differential effects of advancing age on neurotransmitter, cell loss in the substantia nigra and striatum of the C57BL/6N mouse, Brain Res., (in press).Google Scholar