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Research Articles

Differences in the expression of myelopathy in a rat model of chronic spinal cord compression

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Abstract

Context/Objective

The degree of spinal cord compression does not always parallel neurological symptoms. We considered that some compensatory neuroprotective mechanism underlies the expression of this neurological phenotype. Oxygen-regulated-protein 150 (ORP150) is neuroprotective and expressed in neurons in response to neuronal ischemia. We sought to elucidate whether ORP150 expression is associated with the severity and variation of neurological recovery in our rat model of chronic spinal cord compression.

Methods

We made a rat model of chronic spinal cord compression inserting an expandable water-absorbing polyurethane sheet. A neurological behavioral assessment of the severity of paralysis was performed for 10 weeks postoperatively. The rat model was defined as two groups: a myelopathy group with decreased locomotor function and an asymptomatic group. At 10 weeks postoperatively, the spinal cord of the cervical segment was resected for histology and qPCR.

Results

Slowly progressive paralysis appeared at 5–10 weeks postoperatively in 53% of the rats with spinal cord compression. The asymptomatic group had no histological changes indicative of myelopathy. Histology and qPCR showed increased expression of ORP150 in the asymptomatic group, but the ratio of ORP150-positive neuron in the two groups was not significantly different.

Conclusion

The expression of ORP150 in neurons associated with spinal cord compression suggested that the spinal cord was under ischemic stress due to compression, but relation to the development of myelopathy was unclear. The results suggested that some other compensatory mechanisms may exist in response to spinal cord compression in asymptomatic rats.

Acknowledgments

We are indebted to Mrs. Ikumi Morita for her excellent technical assistance.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author Contributions

Conception and design: all authors; Acquisition of data: M. Miura., S. Okimatsu., and Y. Shiratani; Analysis and interpretation of data: M. Miura., S, Okimatsu., and Y. Shiratani; Drafting the article: M. Miura. Critically revising the article: M. Hashimoto., T. Furuya. Reviewed submitted version of manuscript: all authors; Statistical analysis: M. Miura, M. Hashimoto.

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