{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:03:13Z","timestamp":1791327793249,"version":"4.3.1"},"reference-count":55,"publisher":"Society for Neuroscience","issue":"8","license":[{"start":{"date-parts":[[2007,8,21]],"date-time":"2007-08-21T00:00:00Z","timestamp":1187654400000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2007,2,21]]},"abstract":"<jats:p>It has been proposed that substance P and calcitonin gene-related peptide (CGRP) are upregulated in low-threshold myelinated primary afferents after certain types of nerve injury, and that release of substance P from these afferents contributes to the resulting tactile allodynia. To test this hypothesis, we looked for neuropeptides in A\u03b2 primary afferent terminals in the ipsilateral gracile nucleus and spinal dorsal horn in three nerve injury models: sciatic nerve transection (SNT), spinal nerve ligation (SNL), and chronic constriction injury (CCI). We also looked for evidence of neurokinin 1 (NK1) receptor internalization in the dorsal horn after electrical stimulation of A\u03b2 afferents. We found no evidence of either substance P or CGRP expression in injured A\u03b2 terminals in the spinal cord in any of the models. Although substance P was not detected in terminals of injured afferents in the gracile nucleus, CGRP was expressed in between 32 and 68% of these terminals, with a significantly higher proportion in the SNL and CCI models, compared with SNT. In addition, we did not detect any A\u03b2-evoked NK1 receptor internalization in neurons from laminas I, III, or IV of the dorsal horn in the CCI or SNL models. These results do not support the proposal that substance P is present at significant levels in the terminals of injured A\u03b2 primary afferents in neuropathic models. They also suggest that any release of substance P from injured A\u03b2 afferents is unlikely to activate NK1 receptors in the dorsal horn or contribute to neuropathic pain.<\/jats:p>","DOI":"10.1523\/jneurosci.5401-06.2007","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T18:59:09Z","timestamp":1172084349000},"page":"2035-2044","source":"Crossref","is-referenced-by-count":39,"title":["Upregulation of Substance P in Low-Threshold Myelinated Afferents Is Not Required for Tactile Allodynia in the Chronic Constriction Injury and Spinal Nerve Ligation Models"],"prefix":"10.1523","volume":"27","author":[{"given":"David I.","family":"Hughes","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dugald T.","family":"Scott","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John 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