1993 Fiscal Year Final Research Report Summary
An expetinental study onthe cause of the compression myelopathy and radiculopathy
| Project/Area Number |
04670907
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Keio University |
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Principal Investigator |
FUJIMURA Yoshikazu Keio University Assistant Professor, 医学部, 講師 (30201750)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA M Keio University Assistant, 医学部, 助手 (30217898)
IWAMOTO Y Keio University Assistant, 医学部, 助手 (10203415)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Compression myelopathy / Spinal motor neuron / Choline acetyltransferase / Immunohistochemistry / Microphotometry |
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| Research Abstract |
The fumctionsl changes of the motor neurons is one of the reasons that compression muslopathy and radiculopathy. Choline acetyltransferase(CAT), the final enzyme in acetylcholine synthesis, is known as the most specific marker for cholinergic meurons and it's expression sensitively reflects motor neuron function. In our study, changes in CAT distribution in the rat spinal cord caused by the chronic or acute compression were investigated by quantitating indirect CAT immunofluorescence of the spinal cord sections using a microphotometru system.Twy mice were used as a chronic compression model. There was th chronic compression at the upper cervical spinal cord, the grage of which increaswd gradually according to their week-age. Twy mice were classified to the three groups as follows by the compression : Group1, mild compression ; Group2, moderate compression ; group3 sever compression. Ther were no differences of the averaged fluorescence intensities of the antero-medial nucleus of the anterior horn. which reflected the concentration of CAT, bbetween creased to 76% of those of Group 1. Acute spinal cord injury at C6 level of rats, produced by the weight-placed method, resulted in a severe motor functional deficit initially, followed by a gradual recovery. At C6 level, the fluorescence intensity of the ventrolateral anterior horn(VLAH), decreased to 50% of that of sham-operated group at 2 days, It then recoverd to 60% at 4 days after injury, and remained umchanged thereafter. Fluorescence intensisies in VLAH at C4-5 and C7-8 levels decreased to 60-70% at 2 days after injury, but it recoverd and increased to 105-120% thereafter. A strong correlation was found betweenthe late excessive recvery of the fluorescence intensity in VLAH both rostral and caudal to the injury and the jotor functional recvery.
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