STUDY DESIGN: Animal experimental study with intervention. OBJECTIVE: The purpose of this study was to elucidate whether local administration of an α-antagonist around the dorsal root ganglion (DRG) suppressed sympathetic nerve sprouting, from the acute to the chronic pain development phase, in a lumbar radiculopathy model using immunohistochemical methods. SUMMARY OF BACKGROUND DATA: The abnormal sympathetic-somatosensory interaction may underlie some forms of neuropathic pain. There were several reports suggesting α-antagonists are effective to treat neuropathic pain. However, its pathophysiological mechanisms remain obscure. METHODS: We used 70 male Sprague-Dawley rats. After root constriction (RC), rats received a series of three local injections of the nonselective α-antagonist phentolamine around the DRG for 3 days. There were three groups of rats: those that were injected from the day of surgery and those injected from day 4 and third group injected from day 11. The control rats were subjected to RC but equal-volume normal saline injections, and the naïve rats were not subjected to any surgical procedures. At the 14th postoperative day, the left L5 DRG was removed, embedded in paraffin, and sectioned. Sections were then immunostained with antibodies to tyrosine hydroxylase (TH). To quantify the extent of the presence of sympathetic nerve fibers, we counted TH-immunoreactive fibers in the DRG using a light microscope equipped with a micrometer graticule. We counted the squares of the graticule, which contained TH-immunoreactive fibers for each of five randomly selected sections of the DRG. RESULTS: In the naïve group, TH-immunoreactive fibers were scarce in the DRG. α-antagonist injections from postoperative day 0 and 4 suppressed sympathetic nerve sprouting compared with the control group. α-antagonist injections from postoperative day 11 had no suppressant effect compared with the control group. CONCLUSION: The α-antagonist administered around the DRG could suppress neural plastic changes in the early phase after nerve injury. LEVEL OF EVIDENCE: N/A.
STUDY DESIGN: Animal experimental study with intervention. OBJECTIVE: The purpose of this study was to elucidate whether local administration of an α-antagonist around the dorsal root ganglion (DRG) suppressed sympathetic nerve sprouting, from the acute to the chronic pain development phase, in a lumbar radiculopathy model using immunohistochemical methods. SUMMARY OF BACKGROUND DATA: The abnormal sympathetic-somatosensory interaction may underlie some forms of neuropathic pain. There were several reports suggesting α-antagonists are effective to treat neuropathic pain. However, its pathophysiological mechanisms remain obscure. METHODS: We used 70 male Sprague-Dawley rats. After root constriction (RC), rats received a series of three local injections of the nonselective α-antagonist phentolamine around the DRG for 3 days. There were three groups of rats: those that were injected from the day of surgery and those injected from day 4 and third group injected from day 11. The control rats were subjected to RC but equal-volume normal saline injections, and the naïve rats were not subjected to any surgical procedures. At the 14th postoperative day, the left L5 DRG was removed, embedded in paraffin, and sectioned. Sections were then immunostained with antibodies to tyrosine hydroxylase (TH). To quantify the extent of the presence of sympathetic nerve fibers, we counted TH-immunoreactive fibers in the DRG using a light microscope equipped with a micrometer graticule. We counted the squares of the graticule, which contained TH-immunoreactive fibers for each of five randomly selected sections of the DRG. RESULTS: In the naïve group, TH-immunoreactive fibers were scarce in the DRG. α-antagonist injections from postoperative day 0 and 4 suppressed sympathetic nerve sprouting compared with the control group. α-antagonist injections from postoperative day 11 had no suppressant effect compared with the control group. CONCLUSION: The α-antagonist administered around the DRG could suppress neural plastic changes in the early phase after nerve injury. LEVEL OF EVIDENCE: N/A.