Is large myelinated fiber loss associated with hyperalgesia in a model of experimental peripheral neuropathy in the rat?

Richard E. Coggeshall, Patrick M. Dougherty, Carolyn M. Pover, Susan M. Carlton

Research output: Contribution to journalArticle

122 Citations (Scopus)

Abstract

Recently it has been shown that placement of 4 loose chromic gut sutures around the rat sciatic nerve produces hyperalgesia. A possible mechanism underlying this hyperalgesia is a preferential loss of large myelinated fibers. A difficulty, however, is that neuropathic symptoms are not static and the time course of the axon loss has not been determined. To remedy this deficit, the present study relates axonal changes to the behavior of the animal at various times after induction of the neuropathy. The findings are that a loss of all axon types, with a preferential loss of large myelinated axons, is associated with the development of heat hyperalgesia. As the axon loss progresses, however, the hyperalgesia lessens. In addition, at 28 days post surgery there are essentially no large myelinated axons in the distal segment, but the signs of hyperalgesia have almost resolved. These findings indicate that the onset of the hyperalgesia is accompanied by a preferential loss of large fibers and by a lesser but still substantial loss of small myelinated and unmyelinated axons. The subsequent course of the hyperalgesia, however, is not in any obvious way related to the proportions of large myelinated fibers in the affected nerve.

Original languageEnglish (US)
Pages (from-to)233-242
Number of pages10
JournalPain
Volume52
Issue number2
DOIs
StatePublished - 1993

Fingerprint

Hyperalgesia
Peripheral Nervous System Diseases
Theoretical Models
Axons
Animal Behavior
Sciatic Nerve
Ambulatory Surgical Procedures
Sutures
Hot Temperature

Keywords

  • Degeneration
  • Electron microscopy
  • Hyperalgesia
  • Peripheral nerve injury
  • Regeneration

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Neuroscience(all)
  • Neurology
  • Pharmacology
  • Clinical Psychology

Cite this

Is large myelinated fiber loss associated with hyperalgesia in a model of experimental peripheral neuropathy in the rat? / Coggeshall, Richard E.; Dougherty, Patrick M.; Pover, Carolyn M.; Carlton, Susan M.

In: Pain, Vol. 52, No. 2, 1993, p. 233-242.

Research output: Contribution to journalArticle

Coggeshall, Richard E. ; Dougherty, Patrick M. ; Pover, Carolyn M. ; Carlton, Susan M. / Is large myelinated fiber loss associated with hyperalgesia in a model of experimental peripheral neuropathy in the rat?. In: Pain. 1993 ; Vol. 52, No. 2. pp. 233-242.
@article{e38ddb2c6ed54bf2b8e94041932eebfc,
title = "Is large myelinated fiber loss associated with hyperalgesia in a model of experimental peripheral neuropathy in the rat?",
abstract = "Recently it has been shown that placement of 4 loose chromic gut sutures around the rat sciatic nerve produces hyperalgesia. A possible mechanism underlying this hyperalgesia is a preferential loss of large myelinated fibers. A difficulty, however, is that neuropathic symptoms are not static and the time course of the axon loss has not been determined. To remedy this deficit, the present study relates axonal changes to the behavior of the animal at various times after induction of the neuropathy. The findings are that a loss of all axon types, with a preferential loss of large myelinated axons, is associated with the development of heat hyperalgesia. As the axon loss progresses, however, the hyperalgesia lessens. In addition, at 28 days post surgery there are essentially no large myelinated axons in the distal segment, but the signs of hyperalgesia have almost resolved. These findings indicate that the onset of the hyperalgesia is accompanied by a preferential loss of large fibers and by a lesser but still substantial loss of small myelinated and unmyelinated axons. The subsequent course of the hyperalgesia, however, is not in any obvious way related to the proportions of large myelinated fibers in the affected nerve.",
keywords = "Degeneration, Electron microscopy, Hyperalgesia, Peripheral nerve injury, Regeneration",
author = "Coggeshall, {Richard E.} and Dougherty, {Patrick M.} and Pover, {Carolyn M.} and Carlton, {Susan M.}",
year = "1993",
doi = "10.1016/0304-3959(93)90136-D",
language = "English (US)",
volume = "52",
pages = "233--242",
journal = "Pain",
issn = "0304-3959",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Is large myelinated fiber loss associated with hyperalgesia in a model of experimental peripheral neuropathy in the rat?

AU - Coggeshall, Richard E.

AU - Dougherty, Patrick M.

AU - Pover, Carolyn M.

AU - Carlton, Susan M.

PY - 1993

Y1 - 1993

N2 - Recently it has been shown that placement of 4 loose chromic gut sutures around the rat sciatic nerve produces hyperalgesia. A possible mechanism underlying this hyperalgesia is a preferential loss of large myelinated fibers. A difficulty, however, is that neuropathic symptoms are not static and the time course of the axon loss has not been determined. To remedy this deficit, the present study relates axonal changes to the behavior of the animal at various times after induction of the neuropathy. The findings are that a loss of all axon types, with a preferential loss of large myelinated axons, is associated with the development of heat hyperalgesia. As the axon loss progresses, however, the hyperalgesia lessens. In addition, at 28 days post surgery there are essentially no large myelinated axons in the distal segment, but the signs of hyperalgesia have almost resolved. These findings indicate that the onset of the hyperalgesia is accompanied by a preferential loss of large fibers and by a lesser but still substantial loss of small myelinated and unmyelinated axons. The subsequent course of the hyperalgesia, however, is not in any obvious way related to the proportions of large myelinated fibers in the affected nerve.

AB - Recently it has been shown that placement of 4 loose chromic gut sutures around the rat sciatic nerve produces hyperalgesia. A possible mechanism underlying this hyperalgesia is a preferential loss of large myelinated fibers. A difficulty, however, is that neuropathic symptoms are not static and the time course of the axon loss has not been determined. To remedy this deficit, the present study relates axonal changes to the behavior of the animal at various times after induction of the neuropathy. The findings are that a loss of all axon types, with a preferential loss of large myelinated axons, is associated with the development of heat hyperalgesia. As the axon loss progresses, however, the hyperalgesia lessens. In addition, at 28 days post surgery there are essentially no large myelinated axons in the distal segment, but the signs of hyperalgesia have almost resolved. These findings indicate that the onset of the hyperalgesia is accompanied by a preferential loss of large fibers and by a lesser but still substantial loss of small myelinated and unmyelinated axons. The subsequent course of the hyperalgesia, however, is not in any obvious way related to the proportions of large myelinated fibers in the affected nerve.

KW - Degeneration

KW - Electron microscopy

KW - Hyperalgesia

KW - Peripheral nerve injury

KW - Regeneration

UR - http://www.scopus.com/inward/record.url?scp=0027461395&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027461395&partnerID=8YFLogxK

U2 - 10.1016/0304-3959(93)90136-D

DO - 10.1016/0304-3959(93)90136-D

M3 - Article

C2 - 8384361

AN - SCOPUS:0027461395

VL - 52

SP - 233

EP - 242

JO - Pain

JF - Pain

SN - 0304-3959

IS - 2

ER -