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Cited by 191Spinal Cord Injury ResearchTactile and Sensory InteractionsNerve injury and regeneration

Cortical and subcortical plasticity in the brains of humans, primates, and rats after damage to sensory afferents in the dorsal columns of the spinal cord.

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Kaas, Jon H., Qi, Hui-Xin, Burish, Mark J., Gharbawie, Omar A., Onifer, Stephen M., Massey, James M.·2008·Experimental Neurology
DOI 10.1016/j.expneurol.2007.06.014PMC PMC2268113
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Abstract

The failure of injured axons to regenerate following spinal cord injury deprives brain neurons of their normal sources of activation. These injuries also result in the reorganization of affected areas of the central nervous system that is thought to drive both the ensuing recovery of function and the formation of maladaptive neuronal circuitry. Better understanding of the physiological consequences of novel synaptic connections produced by injury and the mechanisms that control their formation are important to the development of new successful strategies for the treatment of patients with spinal cord injuries. Here we discuss the anatomical, physiological and behavioral changes that take place in response to injury-induced plasticity after damage to the dorsal column pathway in rats and monkeys. Complete section of the dorsal columns of the spinal cord at a high cervical level in monkeys and rats interrupts the ascending axon branches of low threshold mechanoreceptor afferents subserving the forelimb and the rest of the lower body. Such lesions render the corresponding part of the somatotopic representation of primary somatosensory cortex totally unresponsive to tactile stimuli. There are also behavioral consequences of the sensory loss, including an impaired use of the hand/forelimb in manipulating small objects. In monkeys, if some of the afferents from the hand remain intact after dorsal column lesions, these remaining afferents extensively reactivate portions of somatosensory cortex formerly representing the hand. This functional reorganization develops over a postoperative period of 1 month, during which hand use rapidly improves. These recoveries appear to be mediated, at least in part, by the sprouting of preserved afferents within the cuneate nucleus of the dorsal column-trigeminal complex. In rats, such functional collateral sprouting has been promoted by the post-lesion digestion of the perineuronal net in the cuneate nucleus. Thus, this and other therapeutic strategies have the potential of enhancing sensorimotor recoveries after spinal cord injuries in humans.

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Crossref · 10.1016/j.expneurol.2007.06.014

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  • Failure of transplanted sensory axons to penetrate original lesion sites led to denervation of upstream pathways and inactivation of parts of somatosensory cortex.

    “which lead to denervation of upstream pathways and inactivation of parts of somatosensory cortex (Davies et al., 1999; Kaas et al., 2008).”

    From The Perineuronal ‘Safety’ Net? Perineuronal Net Abnormalities in Neurological Disorders (2018) · cites this paper as Kaas et al., 2008

  • When sensory axons were transplanted into adult rats with dorsal column lesions, neurons were able to sprout and extend their processes to additional denervated areas but failed to penetrate the original lesion sites.

    “When sensory axons were transplanted into adult rats with dorsal column lesions, neurons were able to sprout and extend their processes to additional denervated areas, but failed to penetrate the original lesion sites”

    From The Perineuronal ‘Safety’ Net? Perineuronal Net Abnormalities in Neurological Disorders (2018) · cites this paper as Kaas et al., 2008

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Research works printed but not linked: 4

  1. Golgi C. Rendiconti della Reale Accademia Del Lincei. 1893. Intorno all’origine del quarto nervo cerebrale e una questione isto-fisiologica che a questo argomento si collega; pp. 433–450. [Google Scholar]
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Authors
Kaas, J. H., Qi, H.-X., Burish, M. J., Gharbawie, O. A., Onifer, S. M., & Massey, J. M.
Affiliations
  • Vanderbilt University (US)
  • University of Kentucky (US)
  • University of Louisville (US)
Corresponding author
Kaas, Jon H.
ORCID
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2008-02
Volume
209
Issue
2
Pages
407-416
ISSN
0014-4886 (ISSN-L)
DOI
10.1016/j.expneurol.2007.06.014
PMC
PMC2268113
OpenAlex
W2055508174
Cited by
191
References
97
Citations by year
2026: 1 · 2024: 6 · 2023: 10 · 2022: 6 · 2021: 8 · 2020: 6 · 2019: 9 · 2018: 8 · 2017: 10 · 2016: 9 · 2015: 20 · 2014: 18 · 2013: 11 · 2012: 20
FWCI
1.23
Type
journal article
Language
en
Open access
Licence
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
Christopher and Dana Reeve Foundation (T32 GM07347)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Tactile and Sensory Interactions
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Keywords
spinal cord injury, dorsal column lesion, cortical plasticity, somatosensory cortex, low-threshold mechanoreceptors, collateral sprouting, cuneate nucleus, perineuronal nets, functional reorganization, hand function recovery, sensorimotor recovery
MeSH terms
Afferent Pathways, Animals, Brain, Humans, Neuronal Plasticity, Neurons, Spinal Cord Injuries, Rats

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