Ketamine Depresses Toll-Like Receptor 3 Signaling in Spinal Microglia in a Rat Model of Neuropathic Pain (original) (raw)
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Research Articles| March 09 2011
aDepartment of Anesthesiology, School of Stomatology, and
bDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi’an, PR China
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aDepartment of Anesthesiology, School of Stomatology, and
bDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi’an, PR China
Search for other works by this author on:
bDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi’an, PR China
Search for other works by this author on:
aDepartment of Anesthesiology, School of Stomatology, and
Search for other works by this author on:
bDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi’an, PR China
Search for other works by this author on:
aDepartment of Anesthesiology, School of Stomatology, and
Search for other works by this author on:
aDepartment of Anesthesiology, School of Stomatology, and
Search for other works by this author on:
bDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, Fourth Military Medical University, Xi’an, PR China
Search for other works by this author on:
Neurosignals (2011) 19 (1): 44–53.
Received:
November 16 2010
Accepted:
January 14 2011
Published Online:
March 09 2011
Abstract
Reports suggest that microglia play a key role in spinal nerve ligation (SNL)-induced neuropathic pain, and toll-like receptor 3 (TLR3) has a substantial role in the activation of spinal microglia and the development of tactile allodynia after nerve injury. In addition, ketamine application could suppress microglial activation in vitro, and ketamine could inhibit proinflammatory gene expression possibly by suppressing TLR-mediated signal transduction. Therefore, the present study was designed to disclose whether intrathecal ketamine could suppress SNL-induced spinal microglial activation and exert some antiallodynic effects on neuropathic pain by suppressing TLR3 activation. Behavioral results showed that intrathecal ketamine attenuated SNL-induced mechanical allodynia, as well as spinal microglial activation, in a dose-dependent manner. Furthermore, Western blot analysis displayed that ketamine application downregulated SNL-induced phosphorylated-p38 (p-p38) expression, which was specifically expressed in spinal microglia but not in astrocytes or neurons. Besides, ketamine could reverse TLR3 agonist (polyinosine-polycytidylic acid)-induced mechanical allodynia and spinal microglia activation. It was concluded that intrathecal ketamine depresses TLR3-induced spinal microglial p-p38 mitogen-activated protein kinase pathway activation after SNL, probably contributing to the antiallodynic effect of ketamine on SNL-induced neuropathic pain.
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© 2011 S. Karger AG, Basel
2011
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