期刊
JOURNAL OF NEUROSCIENCE
卷 29, 期 46, 页码 14415-14422出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4569-09.2009
关键词
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资金
- National Institutes for Health [DE017821]
- Medical Research Council, UK
- Wellcome Trust Pain Consortium
- Bogue research fellowship
- Fondation pour la Recherche Medicale
- MRC [G0400572] Funding Source: UKRI
- Medical Research Council [G0400572] Funding Source: researchfish
Partial peripheral nerve injury in adult rats results in neuropathic pain-like hypersensitivity, while that in neonatal rats does not, a phenomenon also observed in humans. We therefore compared gene expression profiles in the dorsal horn of adult and neonatal rats in response to the spared nerve injury (SNI) model of peripheral neuropathic pain. The 148 differentially regulated genes in adult, but not young, rat spinal cords indicate a greater microglial and T-cell response in adult than in young animals. T-cells show a large infiltration in the adult dorsal horn but not in the neonate after SNI. T-cell-deficient Rag1-null adult mice develop less neuropathic mechanical allodynia than controls, and central expression of cytokines involved in T-cell signaling exhibits large relative differences between young and adult animals after SNI. One such cytokine, interferon-gamma (IFN gamma), is upregulated in the dorsal horn after nerve injury in the adult but not neonate, and we show that IFN gamma signaling is required for full expression of adult neuropathic hypersensitivity. These data reveal that T-cell infiltration and activation in the dorsal horn of the spinal cord following peripheral nerve injury contribute to the evolution of neuropathic pain-like hypersensitivity. The neuroimmune interaction following peripheral nerve injury has therefore a substantial adaptive immune component, which is absent or suppressed in the young CNS.
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