Literature DB >> 10924814

Dorsal root section elicits signs of neuropathic pain rather than reversing them in rats with L5 spinal nerve injury.

Sebastian Eschenfelder1, Heinz-Joachim Häbler, Wilfrid Jänig.   

Abstract

Mechanical allodynia- and hyperalgesia-like behavior which develops in rats after L5 spinal nerve lesion has been suggested to be due to ectopic activity in the lesioned afferent neurons originating at the lesion site and/or in the dorsal root ganglion because it is eliminated by section of the dorsal root. Here we reevaluated the effect of a dorsal rhizotomy in rats after L5 spinal nerve lesion. Using calibrated von Frey hairs, paw withdrawal threshold to single stimuli and paw withdrawal incidence to repetitive stimulation were tested before and after nerve section. Neuropathic pain behavior of similar time course and magnitude also developed after cutting the L5 dorsal root, and L5 spinal nerve lesion-induced abnormal behavior could not be reversed by dorsal rhizotomy. The neuropathic pain behavior elicited by dorsal root section also developed when impulse conduction in the dorsal root axons was blocked during rhizotomy by a local anesthetic, i.e. when the immediate injury discharge was prevented from reaching the spinal cord. These results challenge the widely accepted idea that neuropathic pain behavior developing after spinal nerve lesion is dependent on ectopic activity in the lesioned afferent neurons. However, the present results do not rule out the possibility that after the two nerve lesions the mechanisms generating neuropathic pain behavior are different. After dorsal rhizotomy neuropathic pain behavior may be related to deafferentation whereas after spinal nerve lesion it may be caused by ectopic activity.

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Year:  2000        PMID: 10924814     DOI: 10.1016/S0304-3959(00)00285-2

Source DB:  PubMed          Journal:  Pain        ISSN: 0304-3959            Impact factor:   6.961


  8 in total

Review 1.  Growth factors and neuropathic pain.

Authors:  Michael H Ossipov
Journal:  Curr Pain Headache Rep       Date:  2011-06

Review 2.  Mechanisms of neuropathic pain.

Authors:  James N Campbell; Richard A Meyer
Journal:  Neuron       Date:  2006-10-05       Impact factor: 17.173

3.  Increased sensitivity of injured and adjacent uninjured rat primary sensory neurons to exogenous tumor necrosis factor-alpha after spinal nerve ligation.

Authors:  Maria Schäfers; Doo H Lee; Dominik Brors; Tony L Yaksh; Linda S Sorkin
Journal:  J Neurosci       Date:  2003-04-01       Impact factor: 6.167

4.  Local knockdown of the NaV1.6 sodium channel reduces pain behaviors, sensory neuron excitability, and sympathetic sprouting in rat models of neuropathic pain.

Authors:  W Xie; J A Strong; J-M Zhang
Journal:  Neuroscience       Date:  2015-02-14       Impact factor: 3.590

Review 5.  Contribution of the spared primary afferent neurons to the pathomechanisms of neuropathic pain.

Authors:  Tetsuo Fukuoka; Koichi Noguchi
Journal:  Mol Neurobiol       Date:  2002-08       Impact factor: 5.590

6.  Spontaneous Multimodal Neural Transmission Suggests That Adult Spinal Networks Maintain an Intrinsic State of Readiness to Execute Sensorimotor Behaviors.

Authors:  Maria F Bandres; Jefferson Gomes; Jacob G McPherson
Journal:  J Neurosci       Date:  2021-08-11       Impact factor: 6.167

7.  The major brain endocannabinoid 2-AG controls neuropathic pain and mechanical hyperalgesia in patients with neuromyelitis optica.

Authors:  Hannah L Pellkofer; Joachim Havla; Daniela Hauer; Gustav Schelling; Shahnaz C Azad; Tania Kuempfel; Walter Magerl; Volker Huge
Journal:  PLoS One       Date:  2013-08-09       Impact factor: 3.240

8.  Activity-dependent redistribution of Kv2.1 ion channels on rat spinal motoneurons.

Authors:  Shannon H Romer; Adam S Deardorff; Robert E W Fyffe
Journal:  Physiol Rep       Date:  2016-11
  8 in total

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