Journal article
Spinal cord amino acid release and content in an arthritis model : the effects of pretreatment with non-NMDA, NMDA, and NK1 receptor antagonists
Brain research, Vol.627(1), pp.89-103
1993
DOI: 10.1016/0006-8993(93)90752-9
PMID: 7904887
Abstract
An experimental arthritis, induced by injection of the knee joint with kaolin and carrageenan, results in guarding of and decreased weight bearing on the limb. At the time of injection, a transient increased release of all amino acids examined is measurable in samples collected by microdialysis. A second and prolonged increase of aspartate (ASP), glutamate (GLU), and glutamine (GLN) concentrations follows after 3 h. The increased release at time of injection is blocked by microdialysis application of a non-N-methyl-D-aspartate (non-NMDA) or an NMDA receptor antagonist, and the release of ASP, GLU, and GLN in the late phase is blocked by pretreatment with a non-NMDA (CNQX), an NMDA (AP7) or a neurokinin 1 (NK1; CP-96,345) antagonist. Dorsal horn immunoreactive staining of GLU, substance P (SP), and calcitonin gene-related peptide (CGRP) is reflective of the events occurring in the late phase of amino acid release since GLU release is positively correlated with GLU staining density. Increased immunoreactivity for GLU, SP, and CGRP at 8 hr in the arthritic animals is differentially altered by pretreatment of the spinal cord dorsal horn with non-NMDA, NMDA, or NK1 receptor antagonists. The differential staining pattern for GLU, SP, and CGRP, the differential release of ASP and GLU, and the differential activation of the EAA and NK1 receptors implies that ASP, GLU, SP, and CGRP are each involved in the processing of sensory information and that their roles in the central sensitization occurring with the inflammatory process, are unique.
Details
- Title: Subtitle
- Spinal cord amino acid release and content in an arthritis model : the effects of pretreatment with non-NMDA, NMDA, and NK1 receptor antagonists
- Creators
- K. A SLUKA - Univ. Texas medical branch, marine biomedical inst., dep. anatomy neurosci., Galveston TX 77555-0843, United StatesK. N WESTLUND - Univ. Texas medical branch, marine biomedical inst., dep. anatomy neurosci., Galveston TX 77555-0843, United States
- Resource Type
- Journal article
- Publication Details
- Brain research, Vol.627(1), pp.89-103
- Publisher
- Elsevier; London; Amsterdam; New York, NY
- DOI
- 10.1016/0006-8993(93)90752-9
- PMID
- 7904887
- ISSN
- 0006-8993
- eISSN
- 1872-6240
- Language
- English
- Date published
- 1993
- Academic Unit
- Iowa Neuroscience Institute; Nursing; Physical Therapy and Rehabilitation Science; Neuroscience and Pharmacology
- Record Identifier
- 9984040576302771
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