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Reproduction and reconstruction of a medulla spinals sensory cell at the cancer and neuropathic pain in orofacial region

口面部癌症和神经性疼痛脊髓脊髓感觉细胞的复制和重建

基本信息

批准号：
15390622
负责人：
NAKANISHI Osamu
金额：
$ 6.34万
依托单位：
Kyushu Dental College
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

项目摘要

This study was reviewed the mechanism of neuropathic and cancer pain from the glutamate toxicity, a local change of c-fos and neuroplasticity in neuronal damage characteristics, and the input and/or control system in trigeminal ganglion of algesthesia informationMethod: Cancer and neuropathic pain was produced to inject a cancer cell (Walker256B carcinocarcinoma) in a subperiosteum, and to inject silicon in a mandibular canal of rat, respectively. In addition, loop type microdialysis probe was inserted in cavum subarachnoideale from cisterna magna go that tip was located in trigeminal nuclei level.1) Behavior: The algetic behavior were evaluated by the counts of reaction of clinching in a hot box.2) It were measured the glutamate concentration of the dialysate which it obtained using dialysis probe by HPLC-ECD method in cancer and neuropathic pain.3) After cancer and neuropathic pain model preparation, it delivered nucleus tractus spinalis nervi trigemini and made frozen section and reviewed c-fos gene expression by in situ hybridization method.Results: It showed rat of the cancer and the neuropathic pain shortening that pain latency was significant both. As for the alteration of glutamate of the cerebral spiral fluid of nucleus tractus spinalis nervi trigemini part in algetic irritation, it increase significantly in a cancer and neuropathic pain rat. In pathological examination, cancer and neuropathic pain rat was found c-fos gene expression from early stage in caudalis subnuclei of nucleus tractus spinalis nervi trigemini.Summary : It review the gene expression to precede programmed cell death by pain and review synapse regenerative power of lesion. And problems and the point that could be improved became clear toward clinical application. We are convinced that establishment of a high therapy of likelihood can develop it more.

本研究从谷氨酸毒性、c-fos的局部变化和神经可塑性对神经元损伤特征的影响，以及三叉神经节痛觉信息的输入和/或控制系统等方面对神经痛和神经痛的机制进行了综述。方法：在大鼠骨膜下注入癌细胞（Walker256B癌），在下颌管中注射硅。环形微透析探针从大池插入蛛网膜下腔，尖端位于三叉神经核水平。1)行为：通过热箱中粘接反应的计数来评价代数行为。2)采用HPLC-ECD法测定肿瘤和神经性疼痛患者透析探针获得的透析液谷氨酸浓度。3)癌性和神经性疼痛模型制备完成后，传递三叉神经脊髓束核并冰冻切片，原位杂交法检测c-fos基因表达。结果：癌变大鼠和神经性疼痛缩短大鼠均有明显的疼痛潜伏期。三叉神经节脊髓束核部分脑螺旋液谷氨酸在代数刺激下的改变，在癌变和神经性疼痛大鼠中显著增加。在病理检查中，肿瘤和神经性疼痛大鼠三叉神经脊髓束核尾侧亚核早期可见c-fos基因表达。综述了痛觉诱发细胞程序性死亡的基因表达和损伤的突触再生能力。在临床应用中，存在的问题和需要改进的地方变得清晰起来。我们相信，建立一种高可能性的治疗方法可以进一步发展它。