2002 Fiscal Year Final Research Report Summary
The pathogenesis of idiopathic scoliosis: Implication for melatonin and its receptor in the spinal deformities of Hereditary Lordoscoliotic Rabbits (LSR)
| Project/Area Number |
13671548
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Osaka Medical College |
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Principal Investigator |
SEMOTO Yoshihiro Osaka Medical College Faculty of Medicine Associate Professor, 医学部, 助教授 (20171358)
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| Co-Investigator(Kenkyū-buntansha) |
BABA Ichiro Osaka Medical College Faculty of Medicine Assistant Professor, 医学部, 助手 (60330073)
KIN Akihiro Osaka Medical College Faculty of Medicine Associate Professor, 医学部, 講師 (80298760)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Hereditary Lordoscoliotic Rabbit (LSR) / melatonin and its receptor / spinal cord / Quantitative RT-PCR |
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| Research Abstract |
We previously reported radiological and histological studies investigating the etiology of spinal deformities in a breed of Japanese White Rabbit, the Hereditary Lordoscoliotic Rabbit (LSR). These animals develop thoracic lordoscoliosis during growth and as such can be used as a model for human idiopathic scoliosis. While previous studies in chickens have established that pinealectomy produces scoliosis, the cause of the condition is yet to be fully elucidated. Thus, serum melatonin levels in LSRs were measured by radioimmunoassay to investigate the association between melatonin and the spinal deformities in LSR. Serum melatonin levels in LSRs were significantly higher than those of controls for each time point examined for animals aged from 4 through to 16 weeks. This finding suggests that alterations in serum melatonin levels in LSR are the result of a feedback mechanism associated with the defective functioning of melatonin receptors. We detected the expression of melatonin receptor mRNA in rabbit spinal cord. No significant quantitative differences were found in the level of expression of melatonin receptor mRNA in the spinal cord between LSRs and controls. In relation to the present study, we suggest that causes of spinal deformities in LSR could be due to the contribution of melatonin receptors as well as that of altered serum melatonin levels in LSR.
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