Lumbar 5 ventral root transection-induced upregulation of nerve growth factor in sensory neurons and their target tissues: a mechanism in neuropathic pain

Li, Li, Xian, Cory, J., Zhong, Jin-Hua and Zhou, Xin-Fu (2003) Lumbar 5 ventral root transection-induced upregulation of nerve growth factor in sensory neurons and their target tissues: a mechanism in neuropathic pain. Molecular and Cellular Neuroscience, 23 2: 232-250. doi:10.1016/S1044-7431(03)00062-9


Author Li, Li
Xian, Cory, J.
Zhong, Jin-Hua
Zhou, Xin-Fu
Title Lumbar 5 ventral root transection-induced upregulation of nerve growth factor in sensory neurons and their target tissues: a mechanism in neuropathic pain
Journal name Molecular and Cellular Neuroscience   Check publisher's open access policy
ISSN 1044-7431
1095-9327
Publication date 2003-06-01
Sub-type Article (original research)
DOI 10.1016/S1044-7431(03)00062-9
Volume 23
Issue 2
Start page 232
End page 250
Total pages 19
Place of publication San Diego ; Sydney
Publisher Academic Press
Language eng
Subject 110904 Neurology and Neuromuscular Diseases
Abstract We have previously demonstrated that profound and persistent neuropathic pain as displayed by mechanical and cold allodynia and thermal hyperalgesia can be produced by a lumbar 5 ventral root transection (L5 VRT) model in adult rats in which only the motor nerve fibers were injured without axotomy of sensory neurons. However, the underlying mechanisms remain to be determined. In this study, by examining its changes in expression and by inhibiting its functions using a neutralizing antibody, we have investigated whether nerve growth factor (NGF), a neurotrophic factor known to have a function in regulating nerve injury-induced pain, is involved in the development of neuropathic pain induced by L5 VRT. Motor nerve injury by L5 VRT resulted in a de novo expression of NGF mRNA in a subpopulation of small sensory neurons and pericellular satellite cells in ipsilateral L5 dorsal root ganglion. NGF protein expression was also increased by sensory neurons with various sizes and by keratinocytes in the target tissue ipsilateral skin. Systemic administration of NGF antiserum twice within 17 days markedly attenuated L5 VRT-induced mechanical allodynia but not the cold allodynia and thermal hyperalgesia. These findings suggest that NGF is an important pain mediator in the generation of mechanical sensitivity induced by L5 VRT.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
Queensland Brain Institute Publications
 
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