Peripheral Mechanisms of Neuropathic Pain — Involvement of Lysophosphatidic Acid Receptor-Mediated Demyelination

Molecular Pain - 2008
Hiroshi Ueda1
1Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1–14 Bunkyomachi, Nagasaki 852-8521, Japan

Tóm tắt

Recent advances in pain research provide a clear picture for the molecular mechanisms of acute pain; substantial information concerning plasticity that occurs during neuropathic pain has also become available. The peripheral mechanisms responsible for neuropathic pain are found in the altered gene/protein expression of primary sensory neurons. With damage to peripheral sensory fibers, a variety of changes in pain-related gene expression take place in dorsal root ganglion neurons. These changes, or plasticity, might underlie unique neuropathic pain-specific phenotype modifications — decreased unmyelinated-fiber functions, but increased myelinated A-fiber functions. Another characteristic change is observed in allodynia, the functional change of tactile to nociceptive perception. Throughout a series of studies, using novel nociceptive tests to characterize sensory-fiber or pain modality-specific nociceptive behaviors, it was demonstrated that communication between innocuous and noxious sensory fibers might play a role in allodynia mechanisms. Because neuropathic pain in peripheral and central demyelinating diseases develops as a result of aberrant myelination in experimental animals, demyelination seems to be a key mechanism of plasticity in neuropathic pain. More recently, we discovered that lysophosphatidic acid receptor activation initiates neuropathic pain, as well as possible peripheral mechanims of demyelination after nerve injury. These results lead to further hypotheses of physical communication between innocuous Aβ- and noxious C- or Aδ-fibers to influence the molecular mechanisms of allodynia.

Từ khóa


Tài liệu tham khảo

10.1016/j.neuron.2007.07.016

10.1038/nn942

10.1016/j.pharmthera.2005.06.003

10.1016/j.neuron.2007.07.008

10.1016/j.neuron.2006.09.021

10.1016/S0140-6736(99)01307-0

10.1124/jpet.106.103614

10.1093/bja/87.1.12

10.1186/1744-8069-3-14

10.1016/j.neuron.2007.07.012

10.1186/1744-8069-3-9

10.1016/j.brainresrev.2004.07.004

10.1038/ncpneuro0113

10.1254/jphs.CRJ06008X

10.1124/jpet.103.060335

10.1093/nar/gnh044

10.1016/S0196-9781(00)00262-X

10.1038/270741a0

10.1007/BF00687400

Inoue M, 1999, J Pharmacol Exp Ther, 291, 308

10.1016/S0896-6273(00)81003-X

10.1046/j.1460-9568.1998.00355.x

10.1016/0304-3959(90)91074-S

10.1016/S0169-328X(01)00226-1

10.1124/jpet.102.046250

10.1016/0006-8993(95)01150-1

10.1523/JNEUROSCI.0983-04.2004

10.1002/cne.21311

10.1006/exnr.1999.7329

10.1038/35054063

10.1016/j.brainres.2004.07.078

10.1016/S0306-4522(02)00779-0

10.1186/1744-8069-2-25

10.1523/JNEUROSCI.20-19-07279.2000

10.1016/S0304-3959(99)00169-4

10.1186/1744-8069-2-16

10.1002/(SICI)1097-4598(199711)20:11<1468::AID-MUS21>3.0.CO;2-X

10.1016/S0140-6736(05)79485-X

10.1186/1744-8069-1-13

10.1016/j.pain.2007.07.026

10.1113/jphysiol.2006.121483

Ma L, 2007, Society for Neuroscience 2007, Dan Diego, CA, 185

10.1152/jn.1996.76.3.1465

Xie W, 2007, Society for Neuroscience 2007, Dan Diego, CA, 185

10.1007/BF00235972

10.1523/JNEUROSCI.14-06-03655.1994

10.1038/355075a0

10.1111/j.1469-7793.2001.0241g.x

10.1016/S0304-3959(98)00045-1

10.1073/pnas.96.21.12096

10.1016/0304-3959(94)90068-X

10.1016/S0003-9993(98)90421-X

10.1016/j.ejpain.2004.11.005

10.1016/S0896-6273(00)81184-8

10.1042/bj2910677

10.1055/s-0038-1666902

10.1038/nrc1143

10.1097/00001756-200212030-00002

10.1038/nn1157

10.1177/1073858402238513

10.1146/annurev.biochem.73.011303.073731

10.1016/j.bbamem.2006.09.026

10.1016/S0169-328X(99)00333-2

10.1016/S0304-3940(99)00464-4

10.1254/jjp.87.104

10.1254/jjp.83.161

10.1038/40187

10.1073/pnas.96.9.5233

10.1038/nrd1719

10.1074/jbc.M211175200

10.1038/nm1060

10.1016/j.neuint.2006.09.003

10.1083/jcb.200204026

10.1152/ajpcell.1997.272.4.C1380

10.1248/bpb.27.1168

10.1073/pnas.91.8.3142

10.1038/ncb1089

10.1074/jbc.M606504200

10.1016/j.neuroscience.2007.12.041

10.1016/j.nbd.2004.09.019

10.1007/BF01191213

10.1523/JNEUROSCI.21-13-04649.2001

10.1124/mol.64.4.994

10.1002/jnr.21220

10.1083/jcb.200702102

10.1523/JNEUROSCI.2806-05.2006

10.1016/B0-443-07287-6/50063-1

10.1016/S0304-3940(96)13109-8

Thông tin
Thông tin xuất bản

Molecular Pain

Thông tin tác giả