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Peripheral contributions to the mechanical hyperalgesia following a lumbar 5 spinal nerve lesion in rats

 J.H. Jang  ;  B.H. Lee  ;  T.S. Nam  ;  J.W. Kim  ;  D.W. Kim  ;  J.W. Leem 
 NEUROSCIENCE, Vol.165(1) : 221-232, 2010 
Journal Title
Issue Date
Action Potentials ; Animals ; Electric Stimulation ; Hyperalgesia/physiopathology* ; Lumbosacral Region ; Male ; NerveFibers, Unmyelinated/physiology ; Rats ; Rats, Wistar ; SpinalNerves/injuries ; SpinalNerves/physiopathology* ; Touch
nerve injury ; antidromic stimulation ; mechanical hyperalgesia ; neuropathic pain ; injury discharge ; Wallerian degeneration.
Using lumbar 5 (L5) dorsal root rhizotomy-bearing rats, we examined the extent to which L5 spinal nerve lesion (SNL)-induced mechanical hyperalgesia was governed by two peripheral components, that is Wallerian degeneration (WD) and peripherally-propagating injury discharge (PID). The contribution of WD to SNL-induced hyperalgesia was studied by excluding PID with lidocaine treatment that blocked nerve conduction temporarily, but completely at the time of injury, whereas PID was examined separately by using brief tetanic electrical stimulation of the spinal nerve mimicking PID. Following the disappearance of L5 rhizotomy-induced transient hyperalgesia, L5 SNL resulted in long-lasting mechanical hyperalgesia as early as one day post-SNL despite a PID block, highlighting the role of WD. In a comparative experiment, a delayed onset of hyperalgesia (7 days) was measured in L3 rhizotomy-bearing rats following L3 SNL with a PID block, in which injured fiber (L3) was separated from intact fibers (L4 and L5) anatomically until they meet at the peripheral terminals, supporting the importance of interactions between degenerating and adjacent intact fibers for WD-induced hyperalgesia. Tetanic electrical stimulation of decentralized L5 spinal nerve resulted in mechanical hyperalgesia developing within 1 day and persisting for 7 days. This hyperalgesia was prevented by lidocaine blockade of the L5 nerve, and was unaffected by lidocaine blockades of the central inputs from L3 and L4 fibers during L5 nerve stimulation, suggesting the mediation of PID-induced hyperalgesia by sensitization, not activation, of peripheral terminals of adjacent intact afferents. The similar hyperalgesia was also observed following electrical stimulation of decentralized L3 spinal nerve. Prior elimination of L4 C-fibers by local capsaicin prevented hyperalgesia induced either by L5 SNL with a PID block or by L5 nerve stimulation. These results suggest that neighboring C-afferents remaining intact after partial nerve injury play a critical role in the development of mechanical hyperalgesia through interaction with degenerating afferents, and also via peripheral sensitization by PID
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1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Dong Wook(김동욱) ORCID logo https://orcid.org/0000-0002-5025-1532
Kim, Jeong Won(김정원)
Nam, Taick Sang(남택상)
Lee, Bae Hwan(이배환) ORCID logo https://orcid.org/0000-0003-4719-9021
Leem, Joong Woo(임중우) ORCID logo https://orcid.org/0000-0002-1605-2230
Jang, Jun Ho(장준호)
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