J Korean Orthop Assoc.
2004 Dec;39(7):736-744.
Differential Expression of Somatostatin Receptor Subtype 2 in Dorsal Root Ganglia after Ischemic Injury in the Rat
- Affiliations
-
- 1Department of Orthopaedic Surgery, Kangnam Sacred Heart Hospital, Hallym University School of Medicine, Seoul, Korea. happyshoulder@yahoo.co.kr
- 2Department of Anatomy, College of Medicine, Hallym University, Chunchon, Korea.
Abstract
- PURPOSE
The somatostatin has been suggested to play a role in the transmission of neurotransmitters and the modulation of pain. Therefore, this study was carried out to investigate the spatial and temporal alterations of sstr2 (somatostatin receptors 2) immunoreactivity after an ischemic injury in rats. MATERIALS AND METHODS: Fifty-five rats (Sprague-Dawley, 200-250 g) were assigned to the experimental group, the other five to the control group. In the experimental group, an occlusion of the left common iliac artery was made using an aneurysm clip. Ten groups were classified according to the time after ischemiareperfusion. Dorsal root ganglia (DRG) cells in the L4, L5, L6 levels of the spinal cord, from the rats were examined the sstr2 using an immunohistochemistry technique. RESULTS: The sstr2A/B immunoreactivity (IR) appeared in the DRG after ischemia-reperfusion. The number of sstr2A- and sstr2B-IR neurons were markedly lower in the group of rats 12 hours after ischemia-reperfusion. In the group of rats one day after ischemia-reperfusion, the sstr2A- and sstr2B-IR neurons began to recover in both number and immunoreactivity. Furthermore, 3 days after ischemia-reperfusion, sstr2A/B immunoreactivity decreased in number and immunoreactivity, and 7 days after ischemia-reperfusion, very weak immunoreactivity was observed in the cytoplasm. CONCLUSION: The sstr2A/B immunoreactivity of the DRG exhibited different appearance according to the post-traumatic compartment syndrome or ischemic injury of the leg. In addition, the chronological alterations of sstr2A and sstr2B immunoreactivities may be important in controlling the pain after a transient ischemia-reperfusion event.