{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,18]],"date-time":"2026-07-18T06:38:34Z","timestamp":1784356714749,"version":"3.55.0"},"reference-count":52,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2004,11,30]],"date-time":"2004-11-30T00:00:00Z","timestamp":1101772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Peripheral Nervous Sys"],"published-print":{"date-parts":[[2004,12]]},"abstract":"<jats:p><jats:bold>Abstract\u2003<\/jats:bold> Diabetic neuropathy (DN) is a complication of diabetes that affects the distal terminals of lengthy\u2010projecting sensory axons. To determine whether diabetes\u2010induced axonal degeneration induces gene expression similar to nerve injury, the expression of activating transcription factor 3 (ATF3) by primary sensory neurons was examined in an experimental mouse model of DN. Diabetes was induced using streptozotocin in C57BL\/6 mice, and ATF3 expression in lumbar dorsal root ganglia was assessed at different time points and correlated with the markers of unmyelinated and myelinated neuronal populations. ATF expression was first evident 3 weeks after diabetes induction in both small unmyelinated and large myelinated neurons, but it was more prevalent in larger neurons. At 6 weeks, ATF3 was expressed by neurons among smaller size ranges, but this shift occurred principally within myelinated populations. The retrograde labeling of neurons innervating the flank and paw skin using Fluoro\u2010Gold labeled appropriate percentages of ATF3\u2010positive neurons at 3 weeks, suggesting ATF3 is expressed by neurons capable of transporting substances. However, the percentage of double\u2010labeled neurons was substantially reduced at 6 weeks, suggesting this capacity decreases during disease progression. Finally, behavioral responses to noxious cutaneous stimuli were assessed. Although no differences to radiant heat were observed, diabetic mice developed severe mechanical hypoalgesia 4\u20135 weeks after diabetes induction. These results demonstrate that the diabetes\u2010induced damage of sensory axons can induce the expression of genes linked to peripheral nerve injury and may identify neurons undergoing nerve damage. Finally, the ability to detect sensory deficits in diabetic mice occurs after the expression of injury\u2010related gene ATF3, suggesting that nerve damage may be underway prior to the appearance of behavioral deficits.<\/jats:p>","DOI":"10.1111\/j.1085-9489.2004.09404.x","type":"journal-article","created":{"date-parts":[[2004,11,30]],"date-time":"2004-11-30T14:53:52Z","timestamp":1101826432000},"page":"242-254","source":"Crossref","is-referenced-by-count":32,"title":["Diabetes\u2010induced expression of activating transcription factor 3 in mouse primary sensory neurons"],"prefix":"10.1111","volume":"9","author":[{"given":"Douglas E.","family":"Wright","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janelle M.","family":"Ryals","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth 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