A Mouse Model of Photochemically Induced Spinal Cord Injury.
10.3340/jkns.2009.46.5.479
- Author:
Min Sheng PIAO
1
;
Jung Kil LEE
;
Jae Won JANG
;
Soo Han KIM
;
Hyung Seok KIM
Author Information
1. Department of Neurosurgery, Chonnam National University Medical School & Research Institute of Medical Sciences, Gwangju, Korea. jkl@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Photochemical;
Spinal cord Injury;
Mouse
- MeSH:
Animals;
Cold Temperature;
Female;
Hindlimb;
Horns;
Humans;
Injections, Intraperitoneal;
Joints;
Light;
Lighting;
Mice;
Nerve Fibers, Myelinated;
Nervous System;
Rats;
Rose Bengal;
Spinal Cord;
Spinal Cord Injuries
- From:Journal of Korean Neurosurgical Society
2009;46(5):479-483
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: A mouse model of spinal cord injury (SCI) could further increase our basic understanding of the mechanisms involved in injury and repair of the nervous system. The purpose of this study was to investigate whether methods used to produce and evaluate photochemical graded ischemic SCI in rats, could be successfully adapted to mice, in a reliable and reproducible manner. METHODS: Thirty female imprinting control region mice (weighting 25-30 g, 8 weeks of age) were used in this study. Following intraperitoneal injection of Rose bengal, the translucent dorsal surface of the T8-T9 vertebral laminae of the mice were illuminated with a fiber optic bundle of a cold light source. The mice were divided into three groups; Group 1 (20 mg/kg Rose bengal, 5 minutes illumination), Group 2 (20 mg/kg Rose bengal, 10 minutes illumination), and Group 3 (40 mg/kg Rose bengal, 10 minutes illumination). The locomotor function, according to the Basso-Beattie-Bresnahan scale, was assessed at three days after the injury and then once per week for four weeks. The animals were sacrificed at 28 days after the injury, and the histopathology of the lesions was assessed. RESULTS: The mice in group 1 had no hindlimb movement until seven days after the injury. Most mice had later recovery with movement in more than two joints at 28 days after injury. There was limited recovery of one joint, with only slight movement, for the mice in groups 2 and 3. The histopathology showed that the mice in group 1 had a cystic cavity involving the dorsal and partial involvement of the dorsolateral funiculi. A larger cavity, involving the dorsal, dorsolateral funiculi and the gray matter of the dorsal and ventral horns was found in group 2. In group 3, most of the spinal cord was destroyed and only a thin rim of tissue remained. CONCLUSION: The results of this study show that the photochemical graded ischemic SCI model, described in rats, can be successfully adapted to mice, in a reliable and reproducible manner. The functional deficits are correlated an increase in the irradiation time and, therefore, to the severity of the injury. The photothrombotic model of SCI, in mice with 20 mg/kg Rose bengal for 5 minutes illumination, provides an effective model that could be used in future research. This photochemical model can be used for investigating secondary responses associated with traumatic SCI.
