Genetic analysis of neuropathic pain-like behavior following peripheral nerve injury suggests a role of the major histocompatibility complex in development of allodynia
(2008) In Pain 136(3). p.313-319- Abstract
- Neuropathic pain is a common consequence of damage to the nervous system. We here report a genetic analysis of development of neuropathic pain-like behaviors after unilateral photochemically-induced ischemic sciatic nerve injury in a panel of inbred rat strains known to display different susceptibility to autoimmune neuroinflammation. Pain behavior was initially characterized in Dark-Agouti (DA; RT1(avl)), Piebald Virol Glaxo (PVG; RT1(c)), and in the major histocompatibility complex (MHC)-congenic strain PVG-RT1(avl). All strains developed mechanical hypersensitivity (allodynia) following nerve injury. However, the extent and duration of allodynia varied significantly among the strains, with PVG displaying more severe allodynia compared... (More)
- Neuropathic pain is a common consequence of damage to the nervous system. We here report a genetic analysis of development of neuropathic pain-like behaviors after unilateral photochemically-induced ischemic sciatic nerve injury in a panel of inbred rat strains known to display different susceptibility to autoimmune neuroinflammation. Pain behavior was initially characterized in Dark-Agouti (DA; RT1(avl)), Piebald Virol Glaxo (PVG; RT1(c)), and in the major histocompatibility complex (MHC)-congenic strain PVG-RT1(avl). All strains developed mechanical hypersensitivity (allodynia) following nerve injury. However, the extent and duration of allodynia varied significantly among the strains, with PVG displaying more severe allodynia compared to DA rats. Interestingly, the response of PVG-RT1(avR1) was similar to that of DA, suggesting regulation by the MHC locus. This notion was subsequently confirmed in an F2 cohort derived from crossing of the PVG and PVG-RT1(avl) strains, where allodynia was reduced in homozygous or heterozygous carriers of the RT1(avl) allele in comparison to rats homozygous for the RT1(c) allele. These results indicate that certain allelic variants of the MHC could influence susceptibility to develop and maintain neuropathic pain-like behavior following peripheral nerve injury in rats. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1186632
- author
- Dominguez, Cecilia A ; Lidman, Olle ; Hao, Jing-Xia ; Diez, Margarita ; Tuncel, Jonatan LU ; Olsson, Tomas ; Wiesenfeld-Hallin, Zsuzsanna ; Piehl, Fredrik and Xu, Xiao-Jun
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- congenic, genetic, neuropathic pain, inbred strains, MHC, immune system
- in
- Pain
- volume
- 136
- issue
- 3
- pages
- 313 - 319
- publisher
- Elsevier
- external identifiers
-
- wos:000257105200012
- scopus:43649084446
- pmid:17764842
- ISSN
- 1872-6623
- DOI
- 10.1016/j.pain.2007.07.009
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
- id
- 9b4c38a0-4d18-4d79-ba34-745792d95659 (old id 1186632)
- date added to LUP
- 2016-04-01 12:16:37
- date last changed
- 2022-01-27 01:23:02
@article{9b4c38a0-4d18-4d79-ba34-745792d95659,
abstract = {{Neuropathic pain is a common consequence of damage to the nervous system. We here report a genetic analysis of development of neuropathic pain-like behaviors after unilateral photochemically-induced ischemic sciatic nerve injury in a panel of inbred rat strains known to display different susceptibility to autoimmune neuroinflammation. Pain behavior was initially characterized in Dark-Agouti (DA; RT1(avl)), Piebald Virol Glaxo (PVG; RT1(c)), and in the major histocompatibility complex (MHC)-congenic strain PVG-RT1(avl). All strains developed mechanical hypersensitivity (allodynia) following nerve injury. However, the extent and duration of allodynia varied significantly among the strains, with PVG displaying more severe allodynia compared to DA rats. Interestingly, the response of PVG-RT1(avR1) was similar to that of DA, suggesting regulation by the MHC locus. This notion was subsequently confirmed in an F2 cohort derived from crossing of the PVG and PVG-RT1(avl) strains, where allodynia was reduced in homozygous or heterozygous carriers of the RT1(avl) allele in comparison to rats homozygous for the RT1(c) allele. These results indicate that certain allelic variants of the MHC could influence susceptibility to develop and maintain neuropathic pain-like behavior following peripheral nerve injury in rats.}},
author = {{Dominguez, Cecilia A and Lidman, Olle and Hao, Jing-Xia and Diez, Margarita and Tuncel, Jonatan and Olsson, Tomas and Wiesenfeld-Hallin, Zsuzsanna and Piehl, Fredrik and Xu, Xiao-Jun}},
issn = {{1872-6623}},
keywords = {{congenic; genetic; neuropathic pain; inbred strains; MHC; immune system}},
language = {{eng}},
number = {{3}},
pages = {{313--319}},
publisher = {{Elsevier}},
series = {{Pain}},
title = {{Genetic analysis of neuropathic pain-like behavior following peripheral nerve injury suggests a role of the major histocompatibility complex in development of allodynia}},
url = {{http://dx.doi.org/10.1016/j.pain.2007.07.009}},
doi = {{10.1016/j.pain.2007.07.009}},
volume = {{136}},
year = {{2008}},
}