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To investigate whether the \u03b22 subunit of VGSCs participates in the generation of neuropathic pain, we used the spared nerve injury (SNI) model in rats to examine \u03b22 subunit expression in selectively injured (tibial and common peroneal nerves) and uninjured (sural nerve) afferents. Three days after SNI, immunohistochemistry and Western blot analysis reveal an increase in the \u03b22 subunit in both the cell body and peripheral axons of injured neurons. The increase persists for &gt;4 weeks, although \u03b22 subunit mRNA measured by real-time reverse transcription-PCR and<jats:italic>in situ<\/jats:italic>hybridization remains unchanged. Although injured neurons show the most marked upregulation,\u03b22 subunit expression is also increased in neighboring non-injured neurons and a similar pattern of changes appears in the spinal nerve ligation model of neuropathic pain. That increased \u03b22 subunit expression in sensory neurons after nerve injury is functionally significant, as demonstrated by our finding that the development of mechanical allodynia-like behavior in the SNI model is attenuated in \u03b22 subunit null mutant mice. Through its role in regulating the density of mature VGSC complexes in the plasma membrane and modulating channel gating, the \u03b22 subunit may play a key role in the development of ectopic activity in injured and non-injured sensory afferents and, thereby, neuropathic pain.<\/jats:p>","DOI":"10.1523\/jneurosci.3066-05.2005","type":"journal-article","created":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T20:38:55Z","timestamp":1132778335000},"page":"10970-10980","source":"Crossref","is-referenced-by-count":109,"title":["Upregulation of the Voltage-Gated Sodium Channel \u03b22 Subunit in Neuropathic Pain Models: Characterization of Expression in Injured and Non-Injured Primary Sensory 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