• Yoshinori Terashima, Mikito Kawamata, Tsuneo Takebayashi, Satoshi Tanaka, Katsumasa Tanimoto, and Toshihiko Yamashita.
• Department of Orthopedic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan. y.terashima@sapmed.ac.jp
• Pain. 2011 May 1; 152 (5): 1024-32.

AbstractLittle is known about the pathophysiological mechanisms of radicular pain. We investigated changes in synaptic transmission of substantia gelatinosa (SG) neurons after an injury to the L5 nerve root using in vivo patch-clamp recording. A total of 141 SG neurons were recorded at L4 and L5 segmental levels of the spinal cord in root constriction rats and sham-operated control rats. At L4 and L5 segmental levels, SG neurons without a receptive field were observed only in root constriction rats, and the frequencies of spontaneous action potential firings in SG neurons were higher in the root constriction group than in the control group. At the L5 segmental level, the frequencies and amplitudes of spontaneous excitatory postsynaptic currents (EPSCs) as well as the proportion of multireceptive neurons among SG neurons was higher in the root constriction group than in the control group. At the L4 segmental level, the frequencies and amplitudes of spontaneous EPSCs were increased in the root constriction group, but the proportions of cell types did not change. The mean amplitudes of EPSCs evoked by mechanical stimuli at L4 and L5 segmental levels were larger in the root constriction group than in the control group. The results indicated that injuring the nerve root led to characteristic excitatory synaptic transmission in SG neurons at each segmental level and changed sensory processing in SG neurons at the segment to which the injured nerve projected. These changes could lead to spontaneous pain, mechanical allodynia, and hyperalgesia contributing to the pathogenesis of radicular pain.Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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