title: Changes of cervical dorsal root ganglia induced by compression injury and decompression procedure: a novel rat model of cervical radiculoneuropathy.
abstract: Our study aimed to establish a model of compression injury of cervical dorsal root ganglia (DRG) in the rat and to investigate the pathological changes following compression injury and decompression procedures. Thirty rats were divided into three groups: control group receiving sham surgery, compression group undergoing surgery to place a micro-silica gel on C6 DRG, and decompression group with subsequent decompression procedure. The samples harvested from the different groups were examined with light microscopy, ultrastructural analysis, and horseradish peroxidase (HRP) retrograde tracing techniques. Apoptosis of DRG neurons was demonstrated with TUNEL staining. Changes in PGE2 and PLA2 in DRG neurons were detected with enzyme-linked immunosorbent assay (ELISA). Local expression of vascular endothelial growth factor (VEGF) was monitored with immunohistochemistry. DRG neurons in the compression group became swollen with vacuolar changes in cytoplasm. Decompression procedure partially ameliorated the resultant compression pathology. Ultrastructural examination showed a large number of swollen vacuoles, demyelinated nerve root fibers, absence of Schwann cells, and proliferation in the surrounding connective tissues in the compression group. Compared to the control group, the compression group showed a significant decrease in the number of the HRP-labeled cells and a significant increase in levels of PGE2 and PLA2, in the expression of VEGF protein, and in the number of apoptotic DRG neurons. These findings demonstrate that compression results in local inflammation, followed by increased apoptosis and upregulation of VEGF. We conclude that such a model provides a tool to study the pathogenesis and treatment of cervical radiculoneuropathy.
authors.affiliation: Institute of Spine, Shanghai University of Traditional Chinese Medicine, Shanghai, P. R. China.
authors.forename: Zhan-Ying
authors.initials: ZY
authors.lastname: Tang
authors.forename: Bing
authors.initials: B
authors.lastname: Shu
authors.forename: Xue-Jun
authors.initials: XJ
authors.lastname: Cui
authors.forename: Chong-Jian
authors.initials: CJ
authors.lastname: Zhou
authors.forename: Qi
authors.initials: Q
authors.lastname: Shi
authors.forename: Jonathan
authors.initials: J
authors.lastname: Holz
authors.forename: Yong-Jun
authors.initials: YJ
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis; D019299:Decompression, Surgical; D015232:Dinoprostone / Q000378:metabolism; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000293:injuries* / Q000473:pathology / Q000648:ultrastructure; D006735:Horseradish Peroxidase; D007150:Immunohistochemistry; D008297:Male; D046529:Microscopy, Electron, Transmission; D009408:Nerve Compression Syndromes / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D054467:Phospholipases A2 / Q000378:metabolism; D011843:Radiculopathy / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013194:Staining and Labeling; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D006735:Horseradish Peroxidase; D054467:Phospholipases A2; D015232:Dinoprostone