Metabotropic glutamate receptor-5 and protein kinase C-epsilon increase in dorsal root ganglion neurons and spinal glial activation in an adolescent rat model of painful neck injury.
@article{Weisshaar2010MetabotropicGR,
title={Metabotropic glutamate receptor-5 and protein kinase C-epsilon increase in dorsal root ganglion neurons and spinal glial activation in an adolescent rat model of painful neck injury.},
author={Christine L. Weisshaar and Ling Dong and Alex S. Bowman and Federico M. Perez and Benjamin B. Guarino and Sarah M. Sweitzer and Beth A. Winkelstein},
journal={Journal of neurotrauma},
year={2010},
volume={27 12},
pages={
2261-71
}
}There is growing evidence that neck pain is common in adolescence and is a risk factor for the development of chronic neck pain in adulthood. The cervical facet joint and its capsular ligament is a common source of pain in the neck in adults, but its role in adolescent pain remains unknown. The aim of this study was to define the biomechanics, behavioral sensitivity, and indicators of neuronal and glial activation in an adolescent model of mechanical facet joint injury. A bilateral C6-C7 facet…
31 Citations
Whiplash-like facet joint loading initiates glutamatergic responses in the DRG and spinal cord associated with behavioral hypersensitivity
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Brain‐derived neurotrophic factor is upregulated in the cervical dorsal root ganglia and spinal cord and contributes to the maintenance of pain from facet joint injury in the rat
- BiologyJournal of neuroscience research
- 2013
Changes in BDNF after painful facet joint injury and the effect of spinal BDNF sequestration in partially reducing pain suggest that BDNF signaling contributes to the maintenance of loading‐induced facet pain but that additional cellular responses are also likely involved.
Ablating spinal NK1-bearing neurons eliminates the development of pain and reduces spinal neuronal hyperexcitability and inflammation from mechanical joint injury in the rat.
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Activating transcription factor 4, a mediator of the integrated stress response, is increased in the dorsal root ganglia following painful facet joint distraction
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Gabapentin alleviates facet-mediated pain in the rat through reduced neuronal hyperexcitability and astrocytic activation in the spinal cord.
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Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters
- BiologyNeuroscience Letters
- 2017
The Prostaglandin E2 Receptor, EP2, Is Upregulated in the Dorsal Root Ganglion After Painful Cervical Facet Joint Injury in the Rat
- Biology, MedicineSpine
- 2013
The transient increase in neuronal EP2 suggests, as in other painful joint conditions, that after joint injury nonneuronal cells may migrate to the DRG, some of which likely express EP2.
blation of IB 4 non-peptidergic afferents in the rat facet joint revents injury-induced pain and thalamic hyperexcitability via upraspinal glutamate transporters
- Biology
- 2017
It is suggested that a painful facet injury induces changes extending to supraspinal structures and that IB4-positive afferents in the facet joint may be critical for the development and maintenance of sensitization in the thalamus after a painfulacet joint injury.
A Nociceptive Role for Integrin Signaling in Pain After Mechanical Injury to the Spinal Facet Capsular Ligament
- Biology, MedicineAnnals of Biomedical Engineering
- 2017
It is suggested that integrin subunit β1-dependent pathways may contribute to SP-mediated pain from mechanical injury of the facet capsular ligament through their role in cell adhesion and mechanotransduction.
Development of spinal neuronal hyperexcitability and structural plasticity after cervical facet injury: Implications for modulating persistent pain
- Biology, Medicine
- 2014
Studies in this thesis demonstrate that afferent discharge induced by injurious loading of the facet joint initiates excitatory synaptic and structural changes in the spinal cord that promote neuronal hyperexcitability, but SCS can attenuate persistent pain by reducing spinal hyperexCitability.
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