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Modelling at‐level allodynia after mid‐thoracic contusion in the rat
Journal article   Open access   Peer reviewed

Modelling at‐level allodynia after mid‐thoracic contusion in the rat

Gary H. Blumenthal, Bharadwaj Nandakumar, Ashley K. Schnider, Megan R. Detloff, Jerome Ricard, John R. Bethea and Karen A. Moxon
European journal of pain, v 25(4), pp 801-816
Apr 2021
DOI: https://doi.org/10.1002/ejp.1711
PMID: 33296535
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8318779View
Accepted (AM)Open Access (License Unspecified),  Open

Abstract

Background The rat mid‐thoracic contusion model has been used to study at‐level tactile allodynia, a common type of pain that develops after spinal cord injury (SCI). An important advantage of this model is that not all animals develop hypersensitivity. Therefore, it can be used to examine mechanisms that are strictly related to the development of pain‐like behaviour separately from mechanisms related to the injury itself. However, how to separate animals that develop hypersensitivity from those that do not is unclear. Methods The aims of the current study were to identify where hypersensitivity and spasticity develop and use this information to identify metrics to separate animals that develop hypersensitivity from those that do not to study differences in their behaviour. To accomplish these aims, a grid was used to localize hypersensitivity on the dorsal trunk relative to thoracic dermatomes and supraspinal responses to tactile stimulation were tallied. These supraspinal responses were used to develop a hypersensitivity score to separate animals that develop hypersensitivity, or pain‐like response to nonpainful stimuli. Results Similar to humans, the development of hypersensitivity could occur with the development of spasticity or hyperreflexia. Moreover, the time course and prevalence of hypersensitivity phenotypes (at‐, above‐, or below level) produced by this model were similar to that observed in humans with SCI. Conclusion However, the amount of spared spinal matter in the cord did not explain the development of hypersensitivity, as previously reported. This approach can be used to study the mechanisms underlying the development of hypersensitivity separately from mechanisms related to injury alone. Significance To model at‐level tactile allodynia, rat hypersensitivity was assessed by carefully observing supraspinal responses that are indicative of pain‐like behaviours after mid‐thoracic SCI. By quantifying these supraspinal responses, a hypersensitivity score was developed that models allodynia and was used to separate animals that develop at‐level hypersensitivity from those that did not. Hypersensitivity that included supraspinal responses was localized to thoracic dermatomes T4‐T11 and could be identified by considering only audible vocalisation and avoidance behaviours. Like human allodynia, at‐level hypersensitivity often occurred without hypersensitivity at other levels, was distinguishable from spasticity and hyperreflexia, and developed early after SCI, suggesting that this model could be used to study mechanisms underlying at‐level allodynia.

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Collaboration types
Domestic collaboration
Web of Science research areas
Anesthesiology
Clinical Neurology
Neurosciences
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