Publication | Open Access
Early Withdrawal of Axons from Higher Centers in Response to Peripheral Somatosensory Denervation
31
Citations
47
References
2009
Year
Peripheral Nerve InjuryMassive ReorganizationNeurotransmissionC1 LevelPeripheral NervePeripheral NervesDeafferented BrainstemPeripheral Nervous SystemEarly WithdrawalNeural MechanismNeurologyNeurological FunctionHealth SciencesMedicineHigher CentersRehabilitationNervous SystemSynaptic PlasticityNeurophysiologyNeuroanatomyPhysiologyNeuroscienceCentral Nervous SystemPeripheral Somatosensory Denervation
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.
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