Mechanism of myelopathy and neuronal loss caused, by chronic spinal cord compression in a novel rat model.

新型大鼠模型中慢性脊髓受压引起的脊髓病和神经元损失的机制。

• 批准号: 10671314
• 负责人: KIM Phyo
• 金额: $ 2.3万
• 依托单位: Dokkyo University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1998
• 资助国家: 日本
• 起止时间: 1998 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671314/
• 关键词: cervical myelopathy; rat model.; spinal cord; compression; motor neuron; cell death; 脊髄圧迫; 運動ニューロン; 脊髄断面積; 変形性頚椎症; ミエロパチー

A novel experimental model was developed in the rat to reproduce chronic cervical myelopathy. A thin expanding polymer was installed underneath the cervical laminae without causing immediate injury to the spinal cord. After the operation, motor functions were monitored for 25 weeks; voluntary exercise by cumulative count of revolving cages, and locomotion capability by maximal duration on a rotating treadmill.Immediately after surgery, the two parameters decreased but recovered in two weeks in the compression and in the control (undergoing sham operation) groups. Capability of forced locomotion deteriorated in the compression group with a latency of 17 weeks and progressively thereafter. In the control group, the parameter stayed unchanged throughout 25 weeks. In both groups, amount of voluntary exercise declined gradually in a comparable manner during the observation period.Motor neurons were counted stereologically in continuous sections (thickness and interval :5 μm, 300 slices) at 1,3,9,and 25 weeks after surgery. The neuron count decreased significantly in 9 weeks (-20.3%) and 25 weeks (-35.5%) after compression. Cross sectional area of the cord was reduced by 11.3 % (25 weeks).The model successfully reproduces important characteristics of clinical spondylotic myelopathy, namely, progressive course with an insidious onset, and association of motor neuron loss that precedes the symptoms.

在大鼠中开发了一种新的实验模型来重现慢性脊髓型颈椎病。将薄薄的膨胀聚合物安装在颈椎板下方，不会立即对脊髓造成伤害。术后监测25周的运动功能；通过旋转笼的累积计数来衡量自主运动能力，通过旋转跑步机上的最大持续时间来衡量运动能力。手术后，这两个参数立即下降，但在压缩组和对照组（进行假手术）中两周后恢复。压缩组的强迫运动能力恶化，潜伏期为 17 周，此后逐渐恶化。在对照组中，该参数在 25 周内保持不变。两组患者观察期间自主运动量均逐渐下降，术后1、3、9、25周连续切片（厚度、间隔：5μm，300片）进行体视学计数运动神经元。压缩后 9 周（-20.3%）和 25 周（-35.5%）神经元数量显着减少。脊髓横截面积减少了 11.3%（25 周）。该模型成功地再现了临床脊髓病的重要特征，即隐匿性发作的进行性病程，以及症状出现之前运动神经元丧失的相关性。

项目成果

Kim P, Yoshimoto Y, Iino M, et al: "Increased Calcium Permeability of Sarcolemma during Chronic Vasospasm following Subarachnoid Hemorrhage"J Cereb Blood Flow Met. 16. 334-341 (1996)

Kim P、Yoshimoto Y、Iino M 等人：“蛛网膜下腔出血后慢性血管痉挛期间肌膜的钙渗透性增加”J Cereb Blood Flow Met。

川本俊樹、金彪: "脊髄血管障害 Annual Review神経1999"中外医学社. 10 (1999)

Toshiki Kawamoto、Biao Kane：“脊髓血管疾病年度回顾神经病学 1999”Chugai Igakusha 10 (1999)。

Kim P, Yoshimoto Y, Nakaguchi H, et al: "Increased Sarcolemmal Permeability in the Cerebral Artery during Chronic Spasm. An Assessment using DNA-binding Dyes and Detection of Apoptosis"J. Cereb Blood Flow Met.. 19. 889-897 (1999)

Kim P、Yoshimoto Y、Nakaguchi H 等人：“慢性痉挛期间脑动脉肌膜通透性增加。使用 DNA 结合染料进行评估并检测细胞凋亡”J。

Kim P, Yoshimoto Y, Nakaguchi H, et al.: "Increased Sarcolemmal Permeability in the Cerebral Artery during Chronic Spasm. An Assessnient using DNA-binding Dyes and Detection of Apoptosis."J Cereb Blood Flow Met. 19. 889-897 (1999)

Kim P、Yoshimoto Y、Nakaguchi H 等人：“慢性痉挛期间脑动脉肌膜通透性增加。使用 DNA 结合染料进行评估并检测细胞凋亡。”J Cereb Blood Flow Met。

川本俊樹、金 彪: "脊髄血管障害 Annual Review 神経 1999"中外医学社. 10 (1999)

Toshiki Kawamoto、Biyo Kim：“脊髓血管疾病年度回顾神经病学 1999”Chugai Igakusha 10 (1999)。