| Neural changes in acute arthritis in monkeys. IV. Time-course of amino acid release into the lumbar dorsal horn. | |
| | |
MedLine Citation:
|
PMID: 1638274 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Extracellular levels of amino acids were measured during the development of experimental arthritis in anesthetized monkeys. Levels of glutamate, aspartate, glycine, serine, glutamine, taurine, cysteic acid and asparagine were each measured in consecutive 30 min samples before, during and for several hours after injection of kaolin and carrageenan into the articular capsule of one knee. Samples were obtained via a microdialysis probe placed in the lumbar dorsal horn ipsilateral to the injected knee and assayed using HPLC with fluorescence detection. Glutamate, aspartate, glycine and serine increased transiently following intra-articular injection of inflammatory agents. During this period glutamine levels decreased. A second phase of release then occurred which included more prolonged changes in amino acid levels that were sometimes of greater magnitude than those immediately following the injection. In animals which were later observed to have depletion of SP in the dorsal horn of the inflamed side, taurine levels increased starting after the Glu, Asp and Gly had plateaued at near baseline concentrations. Thus during the first stages of joint inflammation EAAs are released into the dorsal horn, followed by increased levels of IAAs, possibly representing activation of the descending endogenous analgesia system. This phase is followed by a semiacute response consisting in part of increased extracellular levels of SP and Tau. While SP is presumably part of an ascending nociceptive transmission system, Tau could be part of a second system aimed at reducing excessive neural activity including neural transmission resulting in intense maintained pain. |
| | |
Authors:
|
L S Sorkin; K N Westlund; K A Sluka; P M Dougherty; W D Willis |
Related Documents
:
|
2860894 - On the mechanism of enhanced atp formation in hypoxic myocardium caused by glutamic acid. 5124394 - The urinary excretion of orally administered pteroyl-l-glutamic acid by the rat. 8614254 - Role of glutamate in regulating hypothalamic proglucagon-derived peptide secretion in v... 3189784 - Quantitation of aspartate and glutamate in hplc analysis of phenylthiocarbamyl amino ac... 16819954 - Diversity of a stable enrichment culture which is useful for silage inoculant and its s... 16388624 - Synthesis of 2-amino-8-oxodecanoic acids (aodas) present in natural hystone deacetylase... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
|
Title: Brain research. Brain research reviews Volume: 17 ISSN: - ISO Abbreviation: Brain Res. Brain Res. Rev. Publication Date: 1992 Jan-Apr |
Date Detail:
|
Created Date: 1992-09-02 Completed Date: 1992-09-02 Revised Date: 2007-11-14 |
Medline Journal Info:
|
Nlm Unique ID: 8908638 Medline TA: Brain Res Brain Res Rev Country: NETHERLANDS |
Other Details:
|
Languages: eng Pagination: 39-50 Citation Subset: IM |
Affiliation:
|
Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77550-2772. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Acute Disease Amino Acids / metabolism* Animals Arthritis / chemically induced, metabolism* Chromatography, High Pressure Liquid Inflammation / metabolism Injections Lumbosacral Region Macaca fascicularis Movement / physiology Neural Pathways / physiology Spinal Cord / metabolism* Taurine / metabolism Time Factors |
| Grant Support | |
ID/Acronym/Agency:
|
NS01445/NS/NINDS NIH HHS; NS09743/NS/NINDS NIH HHS; NS11255/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Amino Acids; 107-35-7/Taurine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Neural changes in acute arthritis in monkeys. I. Parallel enhancement of responses of spinothalamic ...
Next Document: Vestibular influences on the sympathetic nervous system.