{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T03:02:55Z","timestamp":1791169375072,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T00:00:00Z","timestamp":1147910400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2006,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Sodium channel \u03b24 is a very recently identified auxiliary subunit of the voltage\u2010gated sodium channels. To find the primarily affected gene in Huntington's disease (HD) pathogenesis, we profiled HD transgenic mice using a high\u2010density oligonucleotide array and identified \u03b24 as an expressed sequence tag (EST) that was significantly down\u2010regulated in the striatum of HD model mice and patients. Reduction in \u03b24 started at a presymptomatic stage in HD mice, whereas other voltage\u2010gated ion channel subunits were decreased later. In contrast, spinal cord neurons, which generate only negligible levels of expanded polyglutamine aggregates, maintained normal levels of \u03b24 expression even at the symptomatic stage. Overexpression of \u03b24 induced neurite outgrowth in Neuro2a cells, and caused a thickening of dendrites and increased density of dendritic spines in hippocampal primary neurons, indicating that \u03b24 modulates neurite outgrowth activities. These results suggest that down\u2010regulation of \u03b24 may lead to abnormalities of sodium channel and neurite degeneration in the striatum of HD transgenic mice and patients with HD.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2006.03893.x","type":"journal-article","created":{"date-parts":[[2006,5,18]],"date-time":"2006-05-18T09:51:23Z","timestamp":1147945883000},"page":"518-529","source":"Crossref","is-referenced-by-count":86,"title":["Sodium channel \u03b24 subunit: down\u2010regulation and possible involvement in neuritic degeneration in Huntington's disease transgenic 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