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Updated: Feb 5, 2026

The Spared Nerve Injury SNI Model of Induced Mechanical Allodynia in Mice
Published on: August 18, 2011
NGF and BDNF expression in mouse DRG after spared nerve injury
Yuki Terada1, Shoko Morita-Takemura2, Ayami Isonishi2
1Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634-8521, Japan; Department of Anesthesiology, Nara Medical University, 840, Shijo-cho Kashihara, Nara 634-8522, Japan.
Abstract:
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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