Increase of 200-kDa neurofilament-immunoreactive afferents in the substantia gelatinosa in allodynic rats induced by compression of the dorsal root ganglion.
METHODS
An experimental study on mechanical allodynia, c-Fos expression, and 200-kDa-neurofilament immunoreactive (IR) afferent expression in the substantia gelatinosa related to compression of dorsal root ganglion (DRG).


OBJECTIVE
To evaluate the presence of allodynia in DRG compression model and to demonstrate that the structural changes of spinal dorsal horn related to DRG compression.


BACKGROUND
A previous experimental report has demonstrated that the peripheral nerve injury may trigger some structural changes of the superficial spinal dorsal horn. These changes of the spinal dorsal horn were thought to be important for the modulation of pain sensations such as allodynia.


METHODS
Sixty-eight male rats were used. The left L5 lamina was exposed and a drill hole was made in it. A stainless rod was placed close to the left L5 DRG through the drill hole. Behavioral testing with von Frey filament was performed. On day 28 after surgery, c-Fos expression in the spinal dorsal horn by non-noxious stimulation was examined. L5 spinal cord and bilateral L5 DRG specimens were stained with antibody for 200-kDa neurofilament (RT97). In addition, 2 or 3 spinal cord sections per rats were processed for immunoelectron microscopy.


RESULTS
In the DRG compression group, the mechanical withdrawal threshold was decreased, c-Fos expression by non-noxious stimulation was observed in the spinal dorsal horn, and there were many RT97-IR afferents in the superficial spinal dorsal horn. Immunoelectron microscopic observations showed that RT97-IR terminals made synaptic contact with neurons in the superficial spinal dorsal horn. There were no significant differences in the distribution of RT97-IR neurons in DRG between compression and sham group.


CONCLUSIONS
DRG compression induced allodynia and that RT97-IR afferents increased in the superficial dorsal horn of the spinal cord. The increase of RT97-IR afferents may be related to the mechanisms for the observed allodynia.
Watanabe
Kazuyuki
K
Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, Japan. kazu-w@fmu.ac.jp
Konno
Shin-ichi
S
Sekiguchi
Miho
M
Sasaki
Nobuhisa
N
Honda
Takashi
T
Kikuchi
Shin-ichi
S
D000818:Animals; D000906:Antibodies; D001522:Behavior, Animal; D015415:Biomarkers / Q000378:metabolism; D005727:Ganglia, Spinal / Q000473:pathology*; D007150:Immunohistochemistry; D008297:Male; D016253:Microscopy, Immunoelectron; D009408:Nerve Compression Syndromes / Q000378:metabolism* / Q000473:pathology*; D016900:Neurofilament Proteins / Q000276:immunology / Q000378:metabolism*; D009475:Neurons, Afferent / Q000378:metabolism / Q000648:ultrastructure; D017288:Pain Threshold; D010812:Physical Stimulation; D016760:Proto-Oncogene Proteins c-fos / Q000276:immunology / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013376:Substantia Gelatinosa / Q000166:cytology* / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000648:ultrastructure
D000906:Antibodies; D015415:Biomarkers; D016900:Neurofilament Proteins; D016760:Proto-Oncogene Proteins c-fos; C051774:neurofilament protein H