| Sensitized peripheral nociception in experimental diabetes of the rat. | |
| | |
MedLine Citation:
|
PMID: 20832942 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
|
Painful neuropathy is a common complication of diabetes. Particularly in the early stage of diabetic neuropathy, patients are characterized by burning feet, hyperalgesia to heat, and mechanical stimuli, as if residual nociceptors were sensitized. Such symptoms are barely explained by common pathophysiological concepts of diabetic neuropathy. Diabetes was induced in Wistar rats by streptozotocin (STZ). After 4 weeks behavioral testing (Plantar test, Randall-Selitto) was conducted. Basal and stimulated release of calcitonin gene-related peptide (CGRP), Substance P (SP) and prostaglandin E(2) (PGE(2)) from isolated skin and sciatic nerve were assessed by enzyme immunoassays. Electrophysiological properties of identified nociceptors under hyperglycemic, hypoxic, and acidotic conditions were investigated using the skin-nerve preparation. The diabetic rats showed hyperalgesia to heat and pressure stimulation. The basal CGRP/SP release was reduced, but chemical stimulation with bradykinin induced greater release of SP, CGRP and PGE(2) than in control animals. In contrast, capsaicin-stimulated CGRP release was reduced in sciatic nerves. Hypoxia per se lowered von Frey thresholds of most C-nociceptors to half. Hyperglycemic hypoxia induced ongoing discharge in all diabetic but not control C-fibers which was further enhanced under acidosis. Sensory and neurosecretory nociceptor functions are sensitized in diabetes. Diabetic C-fibers show exaggerated sensitivity to hyperglycemic hypoxia with and without additional acidosis, conditions that are thought to mimic ischemic episodes in diabetic nerves. Ongoing C-fiber discharge is known to induce spinal sensitization. Together with altered receptor and ion channel expressions this may contribute to painful episodes in diabetic neuropathy. |
| | |
Authors:
|
D Fuchs; F Birklein; P W Reeh; S K Sauer |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-15 |
Journal Detail:
|
Title: Pain Volume: 151 ISSN: 1872-6623 ISO Abbreviation: Pain Publication Date: 2010 Nov |
Date Detail:
|
Created Date: 2010-10-15 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 7508686 Medline TA: Pain Country: Netherlands |
Other Details:
|
Languages: eng Pagination: 496-505 Citation Subset: IM |
Copyright Information:
|
Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. |
Affiliation:
|
Department of Physiology & Pathophysiology, University of Erlangen/Nürnberg, Universitätsstr. 17, Erlangen, Germany. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Self-reported somatosensory symptoms of neuropathic pain in fibromyalgia and chronic widespread pain...
Next Document: Dropouts and sub-groups--statistics can help but not cure.