Search tips
Search criteria

Results 1-4 (4)

Clipboard (0)

Select a Filter Below

more »
Year of Publication
Document Types
1.  Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection. 
Annals of the Rheumatic Diseases  1994;53(5):309-314.
OBJECTIVES--To investigate the role of primary afferents, sympathetic postganglionic efferents and descending systems on the central control of peripheral inflammation. METHODS--Acute inflammation was induced by intra-articular injection of kaolin and carrageenan into the knee joint cavity of the rat. Before the induction of the arthritis, a unilateral dorsal rhizotomy, a chemical (phentolamine) and/or surgical sympathectomy, or a spinal transection was performed. Joint inflammation (joint circumference and thermographic readings) and behavioural signs were assessed. RESULTS--Only arthritic animals with a dorsal rhizotomy showed a significant reduction of the inflammatory response compared with control arthritic animals. No significant differences in the inflammatory response occurred following sympathectomy or spinal transection. The animals who received sympathectomy showed similar behavioural manifestations to the arthritic animals. CONCLUSIONS--The central terminals of primary afferents are important in the development of acute joint inflammation since dorsal rhizotomy attenuated the inflammatory response in the knee joint. The sympathetic nervous system is not involved in the acute inflammatory phase of this arthritis model. The central processes controlling acute inflammation involve a local spinal circuit since spinal cord transection at T9 has no effect on the inflammation.
PMCID: PMC1005329  PMID: 8017984
3.  Is there a pathway in the posterior funiculus that signals visceral pain? 
Pain  1996;67(2-3):291-305.
The present report provides evidence that axons in the medial part of the posterior column at T10 convey ascending nociceptive signals from pelvic visceral organs. This evidence was obtained from human surgical case studies and histological verification of the lesion in one of these cases, along with neuroanatomical and neurophysiological findings in animal experiments. A restricted lesion in this area can virtually eliminate pelvic pain due to cancer. The results remain excellent even in cases in which somatic structures of the pelvic body wall are involved. Following this procedure, neurological testing reveals no additional neurological deficit. There is no analgesia to pinprick stimuli applied to the body surface, despite the relief of the visceral pain. Since it is reasonable to attribute the favorable results of limited midline myelotomies to the interruption of axons of visceral nociceptive projection neurons in the posterior column, we have performed experiments in rats to test this hypothesis. The results in rats indicate that the dorsal column does indeed include a nociceptive component that signals pelvic visceral pain. The pathway includes neurons of the postsynaptic dorsal column pathway at the L6-S1 segmental level, axons of these neurons in the fasciculus gracilis, and neurons of the nucleus gracilis and the ventral posterolateral nucleus of the thalamus.
PMCID: PMC3081602  PMID: 8951923
Colorectal distention; Fasciculus gracilis; Limited midline myelotomy; Nucleus gracilis; Postsynaptic dorsal column path; Ventral posterior lateral nucleus
4.  Plasticity in Intact Aδ- and C-Fibers Contributes to Cold Hypersensitivity in Neuropathic Rats 
Neuroscience  2007;150(1):182-193.
Cold hypersensitivity is a common sensory abnormality accompanying peripheral neuropathies and is difficult to treat. Progress has been made in understanding peripheral mechanisms underlying neuropathic pain but little is known concerning peripheral mechanisms of cold hypersensitivity. The aim of this study was to analyze the contribution of uninjured primary afferents to the cold hypersensitivity that develops in neuropathic rats. Rats with a lumbar 5 (L5) and L6 spinal nerve ligation (SNL, Chung model) but not sham, developed mechanical allodynia, evidenced by decreased paw withdrawal thresholds and increased magnitude of response to von Frey stimulation. Cold hypersensitivity also developed in SNL but not sham rats, evidenced by enhanced nociceptive behaviors induced by placement on a cold plate (6 °C) or application of icilin (a transient receptor potential M8 (TRPM8)/transient receptor potential A1 (TRPA1) receptor agonist) to nerve-injured hind paws. Single fiber recordings demonstrated that the mean conduction velocities of intact L4 cutaneous Aδ- and C-fibers were not different between naive and SNL rats; however, mechanical thresholds of the Aδ- but not the C-fibers were significantly decreased in SNL compared with naive. There was a higher prevalence of C-mechanoheat-cold (CMHC) fibers in SNL compared with naive, but the overall percentage of cold-sensitive C-fibers was not significantly increased compared with naive. This was in contrast to the numerous changes in Aδ-fibers: the percentage of L4 cold sensitive Aδ-, but not C-fibers, was significantly increased, the percentage of L4 icilin-sensitive Aδ-, but not C-fibers, was significantly increased, the icilin-induced activity of L4 Aδ-, but not C-fibers, was significantly increased. Icilin-induced activity was blocked by the TRPA1 antagonist Ruthenium Red. The results indicate plasticity in both Aδ- and C-uninjured fibers, but Aδ fibers appear to provide a major contribution to cold hypersensitivity in neuropathic rats.
PMCID: PMC2262053  PMID: 17945425
peripheral neuropathy; sensitization; TRPA1; TRPM8; neuropathic pain; cold allodynia

Results 1-4 (4)