Literature DB >> 33296535

Modelling at-level allodynia after mid-thoracic contusion in the rat.

Gary H Blumenthal1,2, Bharadwaj Nandakumar1,2, Ashley K Schnider2, Megan R Detloff3, Jerome Ricard4, John R Bethea4, Karen A Moxon1,2,5.   

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.
© 2021 European Pain Federation - EFIC®.

Entities:  

Mesh:

Year:  2021        PMID: 33296535      PMCID: PMC8318779          DOI: 10.1002/ejp.1711

Source DB:  PubMed          Journal:  Eur J Pain        ISSN: 1090-3801            Impact factor:   3.931


  55 in total

1.  Spinal cord injuries containing asymmetrical damage in the ventrolateral funiculus is associated with a higher incidence of at-level allodynia.

Authors:  Bradley J Hall; Jason E Lally; Eric V Vukmanic; James E Armstrong; Jason D Fell; Daya S Gupta; Charles H Hubscher
Journal:  J Pain       Date:  2010-03-24       Impact factor: 5.820

2.  Remote activation of microglia and pro-inflammatory cytokines predict the onset and severity of below-level neuropathic pain after spinal cord injury in rats.

Authors:  Megan Ryan Detloff; Lesley C Fisher; Violetta McGaughy; Erin E Longbrake; Phillip G Popovich; D Michele Basso
Journal:  Exp Neurol       Date:  2008-04-20       Impact factor: 5.330

3.  Changes in neuronal receptive field characteristics in caudal brain stem following chronic spinal cord injury.

Authors:  C H Hubscher; R D Johnson
Journal:  J Neurotrauma       Date:  1999-06       Impact factor: 5.269

4.  Transcriptional profiling of spinal cord injury-induced central neuropathic pain.

Authors:  Olivera Nesic; Julieann Lee; Kathia M Johnson; Zaiming Ye; Guo-Ying Xu; Geda C Unabia; Thomas G Wood; David J McAdoo; Karin N Westlund; Claire E Hulsebosch; J Regino Perez-Polo
Journal:  J Neurochem       Date:  2005-10-10       Impact factor: 5.372

5.  Translation of the rat thoracic contusion model; part 1-supraspinally versus spinally mediated pain-like responses and spasticity.

Authors:  S van Gorp; R Deumens; M Leerink; S Nguyen; E A Joosten; M Marsala
Journal:  Spinal Cord       Date:  2014-05-13       Impact factor: 2.772

6.  Changes in electrophysiological properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury.

Authors:  Bryan C Hains; Carl Y Saab; Stephen G Waxman
Journal:  Brain       Date:  2005-08-18       Impact factor: 13.501

Review 7.  Neuropathic pain prevalence following spinal cord injury: A systematic review and meta-analysis.

Authors:  D Burke; B M Fullen; D Stokes; O Lennon
Journal:  Eur J Pain       Date:  2016-06-24       Impact factor: 3.931

8.  Association of pain and CNS structural changes after spinal cord injury.

Authors:  Catherine R Jutzeler; Eveline Huber; Martina F Callaghan; Roger Luechinger; Armin Curt; John L K Kramer; Patrick Freund
Journal:  Sci Rep       Date:  2016-01-06       Impact factor: 4.379

9.  Activation of p38 MAP kinase is involved in central neuropathic pain following spinal cord injury.

Authors:  Eric D Crown; Young Seob Gwak; Zaiming Ye; Kathia M Johnson; Claire E Hulsebosch
Journal:  Exp Neurol       Date:  2008-06-12       Impact factor: 5.330

Review 10.  Mechanisms of chronic central neuropathic pain after spinal cord injury.

Authors:  Claire E Hulsebosch; Bryan C Hains; Eric D Crown; Susan M Carlton
Journal:  Brain Res Rev       Date:  2008-12-25
View more
  1 in total

1.  Hindlimb Somatosensory Information Influences Trunk Sensory and Motor Cortices to Support Trunk Stabilization.

Authors:  Bharadwaj Nandakumar; Gary H Blumenthal; Francois Philippe Pauzin; Karen A Moxon
Journal:  Cereb Cortex       Date:  2021-10-01       Impact factor: 4.861

  1 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.