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Rho kinase inhibitor improves motor dysfunction and hypoalgesia in a rat model of lumbar spinal canal stenosis.
Spine (Phila Pa 1976). 2007 Sep 01; 32(19):2070-5.S

Abstract

STUDY DESIGN

Immunohistochemical and behavioral study using a rat cauda equina compression model.

OBJECTIVE

To investigate, after cauda equina compression by spinal canal stenosis (SCS), Rho activation in the spinal cord and cauda equina, and the effect of intrathecal administration of a Rho kinase inhibitor on hypoalgesia and motor dysfunction.

SUMMARY OF BACKGROUND DATA

Compression of the cauda equina caused by SCS is a common clinical disorder associated with sensory disturbance and intermittent claudication. Cauda equina compression is thought to reduce blood flow and result in nerve degeneration caused by various cytokines. Rho, a member of the small GTPases, is a signal transmitter. It promotes Wallerian degeneration, decreases blood flow in the spinal cord and brain, and increases expression of several cytokines. Currently, Rho kinase inhibitor is used clinically to treat progressive nerve damage due to cerebrovascular disorders. However, its effect for SCS has not been evaluated.

METHODS

Forty-two 6-week-old male Sprague-Dawley rats (200-250 g) were used. For the SCS model (n = 27), a small piece of silicon was placed under the lamina of the fourth lumbar vertebra. In the sham-operated group, laminectomies were performed at L5 only (n = 15). We examined mechanical sensitivity and motor function using von Frey hairs and a treadmill, and immunohistochemically localized Rho in the spinal ventral neurons, axons, and Schwann cells in the cauda equina. We also examined the effects of intrathecally administered Rho kinase inhibitor for hypoalgesia or motor dysfunction caused by SCS.

RESULTS

We observed motor dysfunction and hypoalgesia and activated Rho-immunoreactive cells in spinal ventral neuroreported to induce neurite and axonal outgrowth in the spinal cord and brain after nervous system injury. In addition, 1 report showed that Rho kinase was involved in Wallerian degeneration that was rescued by Rho kinase inhibitor. Furthermore, it is thought that Rho is involved in TNF-alpha and interleukin (IL) production in the central nervous system, and the production was inhibited by administering Rho kinase inhibitor in the central nervous system. Regardns, axons, and Schwann cells in the cauda equina. Intrathecal administration of Rho kinase inhibitor improved mechanical hypoalgesia and motor dysfunction caused by SCS.

CONCLUSION

Activated Rho may play an important role in nerve damage in the cauda equina in SCS. Rho kinase inhibitor may be a useful tool in determining the pathomechanism of cauda equina syndrome caused by SCS.

Authors+Show Affiliations

Department of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17762807

Citation

Ito, Toshinori, et al. "Rho Kinase Inhibitor Improves Motor Dysfunction and Hypoalgesia in a Rat Model of Lumbar Spinal Canal Stenosis." Spine, vol. 32, no. 19, 2007, pp. 2070-5.
Ito T, Ohtori S, Hata K, et al. Rho kinase inhibitor improves motor dysfunction and hypoalgesia in a rat model of lumbar spinal canal stenosis. Spine (Phila Pa 1976). 2007;32(19):2070-5.
Ito, T., Ohtori, S., Hata, K., Inoue, G., Moriya, H., Takahashi, K., & Yamashita, T. (2007). Rho kinase inhibitor improves motor dysfunction and hypoalgesia in a rat model of lumbar spinal canal stenosis. Spine, 32(19), 2070-5.
Ito T, et al. Rho Kinase Inhibitor Improves Motor Dysfunction and Hypoalgesia in a Rat Model of Lumbar Spinal Canal Stenosis. Spine (Phila Pa 1976). 2007 Sep 1;32(19):2070-5. PubMed PMID: 17762807.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rho kinase inhibitor improves motor dysfunction and hypoalgesia in a rat model of lumbar spinal canal stenosis. AU - Ito,Toshinori, AU - Ohtori,Seiji, AU - Hata,Katsuhiko, AU - Inoue,Gen, AU - Moriya,Hideshige, AU - Takahashi,Kazuhisa, AU - Yamashita,Toshihide, PY - 2007/9/1/pubmed PY - 2007/9/19/medline PY - 2007/9/1/entrez SP - 2070 EP - 5 JF - Spine JO - Spine (Phila Pa 1976) VL - 32 IS - 19 N2 - STUDY DESIGN: Immunohistochemical and behavioral study using a rat cauda equina compression model. OBJECTIVE: To investigate, after cauda equina compression by spinal canal stenosis (SCS), Rho activation in the spinal cord and cauda equina, and the effect of intrathecal administration of a Rho kinase inhibitor on hypoalgesia and motor dysfunction. SUMMARY OF BACKGROUND DATA: Compression of the cauda equina caused by SCS is a common clinical disorder associated with sensory disturbance and intermittent claudication. Cauda equina compression is thought to reduce blood flow and result in nerve degeneration caused by various cytokines. Rho, a member of the small GTPases, is a signal transmitter. It promotes Wallerian degeneration, decreases blood flow in the spinal cord and brain, and increases expression of several cytokines. Currently, Rho kinase inhibitor is used clinically to treat progressive nerve damage due to cerebrovascular disorders. However, its effect for SCS has not been evaluated. METHODS: Forty-two 6-week-old male Sprague-Dawley rats (200-250 g) were used. For the SCS model (n = 27), a small piece of silicon was placed under the lamina of the fourth lumbar vertebra. In the sham-operated group, laminectomies were performed at L5 only (n = 15). We examined mechanical sensitivity and motor function using von Frey hairs and a treadmill, and immunohistochemically localized Rho in the spinal ventral neurons, axons, and Schwann cells in the cauda equina. We also examined the effects of intrathecally administered Rho kinase inhibitor for hypoalgesia or motor dysfunction caused by SCS. RESULTS: We observed motor dysfunction and hypoalgesia and activated Rho-immunoreactive cells in spinal ventral neuroreported to induce neurite and axonal outgrowth in the spinal cord and brain after nervous system injury. In addition, 1 report showed that Rho kinase was involved in Wallerian degeneration that was rescued by Rho kinase inhibitor. Furthermore, it is thought that Rho is involved in TNF-alpha and interleukin (IL) production in the central nervous system, and the production was inhibited by administering Rho kinase inhibitor in the central nervous system. Regardns, axons, and Schwann cells in the cauda equina. Intrathecal administration of Rho kinase inhibitor improved mechanical hypoalgesia and motor dysfunction caused by SCS. CONCLUSION: Activated Rho may play an important role in nerve damage in the cauda equina in SCS. Rho kinase inhibitor may be a useful tool in determining the pathomechanism of cauda equina syndrome caused by SCS. SN - 1528-1159 UR - https://www.unboundmedicine.com/medline/citation/17762807/Rho_kinase_inhibitor_improves_motor_dysfunction_and_hypoalgesia_in_a_rat_model_of_lumbar_spinal_canal_stenosis_ L2 - https://doi.org/10.1097/BRS.0b013e318145a502 DB - PRIME DP - Unbound Medicine ER -