• Michiko Hayashi, Yoshinori Kamiya, Hideki Itoh, Tomoko Higashi, Tomoyuki Miyazaki, Kengo Funakoshi, Naoya Yamashita, Yoshio Goshima, Tomio Andoh, Yoshitsugu Yamada, and Takahisa Goto.
• Department of Anesthesiology and Critical Care Medicine, Yokohama City University Graduate School of Medicine, Kanazawa-ku, Yokohama, Japan.
• Neurosci. Res. 2011 Jan 1;69(1):17-24.

AbstractSemaphorins, one of the repulsive axonal guidance factors during development, are produced under pathological conditions in adult animals. In the neuropathic pain state associated with peripheral nerve injury, synaptic reorganization occurs in spinal cord dorsal horn. In the present study, we investigated the roles of intrathecal administration of Sema3A, a secreted semaphorin, in the spinal cord of chronic constriction injury (CCI) model rat. Neuropilin 1 (NPR1) and Plexin A (PlexA), co-receptors of Sema3A, were expressed in the dorsal horn of naïve rats. NPR1, and not PlexA, protein expression increased in the dorsal spinal cord of CCI rats. Recombinant Sema3A protein attenuated mechanical allodynia and heat hyperalgesia in CCI rats, whereas heat-inactivated Sema3A had no effect. Immunohistochemistry revealed that Sema3A partially restored the decrease of isolectin B4-positive unmyelinated nerve terminals in lamina II of the ipsilateral dorsal horn of CCI rats. Contrary to our expectations, Sema3A did not change the distribution of myelinated fibers in lamina II at 7 days after CCI. Those results suggested that the suppressive role for Sema3A in the development of neuropathic pain associated with peripheral nerve injury in adult rats, which seemed to be independent from prevention of the myelinated fiber sprouting into lamina II.Copyright © 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

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