Disk Injury in Rats Produces Persistent Increases in Pain-Related Neuropeptides in Dorsal Root Ganglia and Spinal Cord Glia but Only Transient Increases in Inflammatory Mediators
Dorsal root ganglion
Nerve Injury
DOI:
10.1097/brs.0b013e31820e68c7
Publication Date:
2011-01-12T10:05:42Z
AUTHORS (12)
ABSTRACT
Immunohistological analysis in an injured intervertebral disk (IVD) model.To elucidate and compare rats the behavior of sensory nervous system inflammatory mediators experimentally IVDs.Multiple human animal studies have verified presence nerve fibers IVDs or investigated IVDs, but no vivo study to date has examined relationship between 2.Eight-week-old female were used. In disk-injured group, L5/L6 disks with a 24-gauge needle; simultaneously, neurotracer Fluoro-gold was injected into IVD. The IVD dorsal root ganglia (DRGs) from L1 L6 levels, spinal cord resected at several time points after surgery. Nerve growth factor, tumor necrosis factor (TNF)-α interleukin (IL)-6 production quantified using enzyme-linked immunosorbent assay. DRGs immunostained for calcitonin gene-related peptide, sections ionized calcium-binding adaptor molecule-1 glial fibrillary acidic protein.Nerve TNF-α levels (through 1 week) IL-6 4 days) significantly higher group than noninjured (P < 0.05). However, starting 2 weeks (nerve TNF-α) week (IL-6), differences mediator groups longer significant. contrast, percentage peptide-immunoreactive neurons among Fluoro-gold-labeled DRG neurons, numbers molecule-1-immunoreactive microglia protein-immunoreactive astrocytes horn remained all-time 0.05).Disk injury produces persistent increases neuropeptides glia cord, only transient IVDs.
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