Spinal glial activation and cytokine expression after lumbar root injury in the rat

This study was designed to examine the behaviorial immunohistochemical changes of spinal glial cells and spinal Interleukin (IL)-1beta expression after various nerve root injuries used as models of lumbar radiculopathy. In order to better understand the role of central inflammation in the pathophysi...

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Bibliographic Details
Published in:Spine (Philadelphia, Pa. 1976) Pa. 1976), 2000-05, Vol.25 (10), p.1206-1217
Main Authors: Hashizume, H, DeLeo, J A, Colburn, R W, Weinstein, J N
Format: Article
Language:English
Subjects:
Animals
Antigens, CD
Antigens, Neoplasm
Antigens, Surface
Astrocytes - chemistry
Astrocytes - physiology
Avian Proteins
Basigin
Blood Proteins
Disease Models, Animal
Gait
Ganglia, Spinal - injuries
Ganglia, Spinal - pathology
Inflammation Mediators - metabolism
Interleukin-1 - immunology
Interleukin-1 - metabolism
Ligation
Low Back Pain - immunology
Male
Membrane Glycoproteins - analysis
Microglia - physiology
Motor Neurons - physiology
Neurons, Afferent - physiology
Pain Threshold
Physical Stimulation
Radiculopathy - immunology
Rats
Rats, Sprague-Dawley
Reaction Time
Spinal Cord - cytology
Spinal Cord - immunology
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Summary:This study was designed to examine the behaviorial immunohistochemical changes of spinal glial cells and spinal Interleukin (IL)-1beta expression after various nerve root injuries used as models of lumbar radiculopathy. In order to better understand the role of central inflammation in the pathophysiologic mechanisms that give rise to pain associated with lumbar radiculopathy, this research studied the relationship between pain-related behavior associated with spinal glial activation and IL-1beta expression generated by three types of nerve root injury: loose ligation with chromic gut, loose ligation with silk, and tight ligation with silk. An animal model of lumbar radiculopathy originally described by Kawakami and Weinstein involved loose ligation of unilateral L4-L6 nerve roots with chromic gut. Characterization and establishment of such an animal model of low back pain enables further investigation of the nature of the pathophysiologic mechanisms associated with lumbar radiculopathy in humans. Seventy-three rats were divided into four treatment groups. Chromic group (n = 25): The L5 nerve roots (dorsal and ventral) were exposed by hemilaminectomy and loosely ligated with chromic gut. Tight silk group (n = 18): The exposed L5 nerve roots were tightly ligated extradurally with 5-0 silk suture. Loose silk group (n = 15): two loose ligatures of 5-0 silk were placed around the exposed L5 nerve roots. Sham group (n = 15): the rats were subjected to laminectomy alone for exposing nerve roots. Following surgery, thermal hyperalgesia and mechanical allodynia was assessed time-dependently up to 42 days post operatively. At 1, 3, 7, 14, and 42 days postoperatively, the rats in each group were perfused with fixative. The L5 spinal cord segments was harvested and cryosectioned for glial and cytokine immunohistochemistry. In the chromic and the tight silk group, an immediate and sustained mechanical allodynia was observed in the ipsilateral hind paw up to 35 days postoperatively. The loose silk group also showed an immediate mechanical allodynia that subsided by 14 days postoperatively. Sham-treated animals exhibited mild mechanicalallodynia for the initial 7 days after the surgery. Thermalhyperalgesia was evident in the three primary treatment groups, but not in the sham-treated rats. OX-42 expression was elevated in the gray matter of the L5 spinal section by 3 days in the chromic, the tight silk, and the loose silk groups as compared to the sham group. Astrocytic
ISSN:0362-2436
1528-1159
DOI:10.1097/00007632-200005150-00003