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The Journal of Neuroscience, February 21, 2007, 27(8):2035-2044; doi:10.1523/JNEUROSCI.5401-06.2007

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Behavioral/Systems/Cognitive
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

David I. Hughes, Dugald T. Scott, John S. Riddell, and Andrew J. Todd

Spinal Cord Group, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom

Correspondence should be addressed to Dr. David I. Hughes, Spinal Cord Group, West Medical Building, University of Glasgow, University Avenue, Glasgow G12 8QQ, UK. Email: d.hughes{at}bio.gla.ac.uk

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 Aß 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 Aß afferents. We found no evidence of either substance P or CGRP expression in injured Aß 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 Aß-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 Aß primary afferents in neuropathic models. They also suggest that any release of substance P from injured Aß afferents is unlikely to activate NK1 receptors in the dorsal horn or contribute to neuropathic pain.

Key words: peripheral nerve injury; CGRP; NK1 receptor; neuropathic pain; hyperalgesia; NPY

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Received Dec. 14, 2006; revised Jan. 19, 2007; accepted Jan. 20, 2007.

Correspondence should be addressed to Dr. David I. Hughes, Spinal Cord Group, West Medical Building, University of Glasgow, University Avenue, Glasgow G12 8QQ, UK. Email: d.hughes{at}bio.gla.ac.uk

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