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The Journal of Neuroscience, March 25, 2009, 29(12):3738-3748; doi:10.1523/JNEUROSCI.5388-08.2009

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Development/Plasticity/Repair
Early Withdrawal of Axons from Higher Centers in Response to Peripheral Somatosensory Denervation

Alessandro Graziano and Edward G. Jones

Center for Neuroscience, University of California, Davis, Davis, California 95618

Correspondence should be addressed to Dr. Edward G. Jones, 1544 Newton Court, Davis, CA 95618. Email: ejones{at}ucdavis.edu

The mechanisms responsible for long-term, massive reorganization of representational maps in primate somatosensory cortex after deafferentation are poorly understood. Sprouting of cortical axons cannot account for the extent of reorganization, and withdrawal of axons of deafferented brainstem and thalamic neurons, permitting expression of previously silent synapses, has not been directly demonstrated. This study is focused on the second of these. In monkeys, deafferented for two years by section of the cuneate fasciculus at the C1 level, there was extensive withdrawal of axon terminals from thalamus and cortex, detectable a decade before visible atrophy of their parent neuronal somata in the cuneate nucleus or thalamus. Slow, inexorable progression of lemniscal and thalamocortical axonal withdrawal is a neurodegenerative phenomenon likely to be a powerful inducement to compensatory long-term plasticity, a mechanism that can explain the long-term evolution of cortical reorganization and, with it, phantom sensations in spinal patients and amputees.


Received Nov. 6, 2008; revised Jan. 26, 2009; accepted Feb. 14, 2009.

Correspondence should be addressed to Dr. Edward G. Jones, 1544 Newton Court, Davis, CA 95618. Email: ejones{at}ucdavis.edu




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J. Neurosci., September 23, 2009; 29(38): 12009 - 12019.
[Abstract] [Full Text] [PDF]



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