NGF and BDNF expression in mouse DRG after spared nerve injury
[Display omitted] •Several studies have highlighted the important contribution of the DRG in a non-injured nerve.•We showed that a neurotrophin NGF was downregulated in intact DRG neurons after spared nerve injury.•Downregulation of NGF in intact DRG neurons may contribute to the neuropathic pain. N...
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Published in | Neuroscience letters Vol. 686; pp. 67 - 73 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier B.V
01.11.2018
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Subjects | |
Online Access | Get full text |
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Summary: | [Display omitted]
•Several studies have highlighted the important contribution of the DRG in a non-injured nerve.•We showed that a neurotrophin NGF was downregulated in intact DRG neurons after spared nerve injury.•Downregulation of NGF in intact DRG neurons may contribute to the neuropathic pain.
Neuropathic pain is initiated by a primary lesion in the peripheral nervous system and spoils quality of life. Neurotrophins play important roles in the development and transmission of neuropathic pain. There are conflicting reports that the dorsal root ganglion (DRG) in an injured nerve contribute to neuropathic pain, whereas several studies have highlighted the important contribution of the DRG in a non-injured nerve. Clarifying the role of neurotrophins in neuropathic pain is problematic because we cannot distinguish injured and intact neurons in most peripheral nerve injury models. In the present study, to elicit neuropathic pain, we used the spared nerve injury (SNI) model, in which injured DRG neurons are distinguishable from intact ones, and mechanical allodynia develops in the intact sural nerve skin territory. We examined nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) expression in the DRGs of SNI model mice. NGF and BDNF levels increased in the injured L3 DRG, while NGF decreased in the intact L5 DRG. These data offer a new point of view on the role of these neurotrophins in neuropathic pain induced by peripheral nerve injury. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2018.08.051 |