2009 Fiscal Year Final Research Report
A cell adhesion molecule close homologue of L1 increased in primary afferent terminal contributes to the development and maintenance of neuropathic pain
Project/Area Number |
20790170
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
General anatomy (including Histology/Embryology)
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Research Institution | Hyogo College of Medicine |
Principal Investigator |
YAMANAKA Hiroki Hyogo College of Medicine, 医学部, 講師 (20340995)
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Project Period (FY) |
2008 – 2009
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Keywords | 神経因性疼痛 / 細胞間接着 / 脊髄後角 / シナプス / 形態変化 |
Research Abstract |
The L1 family of cell adhesion molecules (L1-CAMs) is known to regulate various neural functions that are pivotal to nervous system, including cell adhesion, axon guidance and synaptic plasticity. We investigated the involvement of a close homologue of the L1 cell adhesion molecule (CHL1) on neuropathic pain produced in the rat spared nerve injury (SNI) model. SNI induced the expression of CHL1 in L4/5 DRG neurons, particularly in small size injured neurons and in satellite cells. In the spinal cord, CHL1-immunoreactivity increased in laminae I-II of the dorsal horn ipsilateral to the injury. Ultrastructural study clarified the localization of CHL1 in the axon of primary afferents in the ipsilateral dorsal horn. CHL1 immunoreactivites were localized in the adherence such as axon- axon, axon-dorsal horn neurons (dendrite, soma) and axon-glia (astrocyte and microglia). Experimental inhibition of CHL1 adhesion by chronic intrathecal administration of the anti-CHL1 extracellular domain significantly prevented andreversed SNI-induced mechanical allodynia. Thus, alterations of CHL1 may be involved in the structural plasticity that is associated with neuropathic pain.
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Research Products
(22 results)
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[Journal Article] Comparative study of the distribution of the alpha-subunits of voltage-gated sodium channels in normal and axotomized rat dorsal root ganglion neurons.2008
Author(s)
Fukuoka, T., Kobayashi, K., Yamanaka, H., Obata, K., Dai, Y., Noguchi, K.
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Journal Title
J. Comp. Neurol. 510
Pages: 188-206
Peer Reviewed
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[Journal Article] Transforming growth factor-activated kinase 1 induced in spinal astrocytes contributes to mechanical hypersensitivity after nerve injury.2008
Author(s)
Katsura, H., Obata, K., Miyoshi, K., Kondo, T., Yamanaka, H., Kobayashi, K., Dai, Y., Fukuoka, T., Sakagami, M., Noguchi, K.
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Journal Title
Peer Reviewed
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[Journal Article] P2Y12 receptor upregulation in activated microglia is a gateway of p38 signaling and neuropathic pain.2008
Author(s)
Kobayashi, K., Yamanaka, H., Fukuoka, T., Dai, Y., Obata, K., Noguchi, K.
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Journal Title
J. Neurosci. 28
Pages: 2892-2902
Peer Reviewed
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[Journal Article] Phospholipase C and protein kinase A mediate bradykinin sensitization of TRPA1: a molecular mechanism of inflammatory pain.2008
Author(s)
Wang, S., Dai, Y., Fukuoka, T., Yamanaka, H., Kobayashi, K., Obata, K., Cui, X., Tominaga, M., Noguchi, K.
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Journal Title
Brain 131
Pages: 1241-1251
Peer Reviewed
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[Journal Article] Activation of extracellular signal-regulated protein kinase in sensory neurons after noxious gastric distention and its involvement in acute visceral pain in rats.2008
Author(s)
Sakurai, J., Obata, K., Ozaki, N., Tokunaga, A., Kobayashi, K., Yamanaka, H., Dai, Y., Kondo, T., Miyoshi, K., Sugiura, Y., Matsumoto, T., Miwa, H., Noguchi, K.
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Journal Title
Gastroenterology 134
Pages: 1094-1103
Peer Reviewed
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[Journal Article] Differential activation of p38 and extracellular signal-regulated kinase in spinal cord in a model of bee venom-induced inflammation and hyperalgesia.2008
Author(s)
Cui, X.Y., Dai, Y., Wang, S.L., Yamanaka, H., Kobayashi, K., Obata, K., Chen, J., Noguchi, K.
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Journal Title
Peer Reviewed
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[Presentation] Laminae-specific distribution of Nav mRNAs in the rat spinal cord2008
Author(s)
Fukuoka, T., Kobayashi, K., Yamanaka, H., Obata, K., Dai, Y., Noguchi, K.
Organizer
The 38th Annual Meeting of the Society for Neuroscience
Place of Presentation
Washington D.C., U.S.A.
Year and Date
20081115-20081119
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