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Hyperexcitable neurons and altered non-neuronal cells in the compressed spinal ganglion

Robert H. LaMotte^*, Chao MA

Department of Anesthesiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA

摘要

The cell body or soma in the dosal root ganglion (DRG) is normally excitable and this excitability can increase and persistafter an injury of peripheral sensory neurons. In a rat model of radicular pain, an intraforaminal implantation of a rod that chronicallycompressed the lumbar DRG (“CCD” model) resulted in neuronal somal hyperexcitability and spontaneous activity that was accompaniedby hyperalgesia in the ipsilateral hind paw. By the 5th day after onset of CCD, there was a novel upregulation in neuronalexpression of the chemokine, monocyte chemoattractant protein-1 (MCP-1 or CCL2) and also its receptor, CCR2. The neuronsdeveloped, in response to topically applied MCP-1, an excitatory response that they normally do not have. CCD also activated nonneuronalcells including, for example, the endothelial cells as evidenced by angiogenesis in the form of an increased number of capillariesin the DRG after 7 days. A working hypothesis is that the CCD induced changes in neurons and non-neuronal cells that may acttogether to promote the survival of the injured tissue. The release of ligands such as CCL2, in addition to possibly activating nociceptiveneurons (maintaining the pain), may also act to preserve injured cells in the face of ischemia and hypoxia, for example, by promotingangiogenesis. Thus, somal hyperexcitability, as often said of inflammation, may represent a double edged sword.

关键词： radicular pain; dorsal root ganglion; neuronal hyperexcitability

Hyperexcitable neurons and altered non-neuronal cells in the compressed spinal ganglion

Robert H. LaMotte^*, Chao MA

Department of Anesthesiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA

Abstract

The cell body or soma in the dosal root ganglion (DRG) is normally excitable and this excitability can increase and persistafter an injury of peripheral sensory neurons. In a rat model of radicular pain, an intraforaminal implantation of a rod that chronicallycompressed the lumbar DRG (“CCD” model) resulted in neuronal somal hyperexcitability and spontaneous activity that was accompaniedby hyperalgesia in the ipsilateral hind paw. By the 5th day after onset of CCD, there was a novel upregulation in neuronalexpression of the chemokine, monocyte chemoattractant protein-1 (MCP-1 or CCL2) and also its receptor, CCR2. The neuronsdeveloped, in response to topically applied MCP-1, an excitatory response that they normally do not have. CCD also activated nonneuronalcells including, for example, the endothelial cells as evidenced by angiogenesis in the form of an increased number of capillariesin the DRG after 7 days. A working hypothesis is that the CCD induced changes in neurons and non-neuronal cells that may acttogether to promote the survival of the injured tissue. The release of ligands such as CCL2, in addition to possibly activating nociceptiveneurons (maintaining the pain), may also act to preserve injured cells in the face of ischemia and hypoxia, for example, by promotingangiogenesis. Thus, somal hyperexcitability, as often said of inflammation, may represent a double edged sword.

Key words: radicular pain; dorsal root ganglion; neuronal hyperexcitability

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通讯作者：Robert H. LaMotte　　E-mail: robert.lamotte@yale.edu

引用本文：

Robert H. LaMotte, Chao MA. Hyperexcitable neurons and altered non-neuronal cells in the compressed spinal ganglion[J]. 生理学报 2008; 60 (5): 597-602.

Robert H. LaMotte, Chao MA. Hyperexcitable neurons and altered non-neuronal cells in the compressed spinal ganglion. Acta Physiol Sin 2008; 60 (5): 597-602 (in Chinese with English abstract).