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Study of neuroplastic centrally induced bladder hyper activity and gene therapy

神经可塑性中枢性膀胱过度活动症及基因治疗研究

基本信息

批准号：
12671525
负责人：
ISHIZUKA Osamu
金额：
$ 2.5万
依托单位：
SHINSHU UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671525/
关键词：
Bladder Overactivity Central Nervous Disorders Gene Therapy Urinary incontinence rats

项目摘要

We studied the centrally induced bladder hyperactivity by using some disease rat models.Bladder outlet obstruction, such as benign prostatic hypertrophy is becoming common disease, which causes bladder hyperactivity. This hyperactivity may results from the disorders of the central nervous control of the micturition. In this study, we could demonstrate that, at the supraspinal level, tachykinin and α1 adrenoceptors may also be involved in micturition control, especially in the rats with bladder outlet obstruction. The results imply that supraspinal NK receptors and adrenergic receptors are a possible target for drugs aimed for elimination of bladder hyperactivity secondary to bladder outlet obstruction.Locus coerules in pons is one of the important areas to induce the symptoms of Parkinson's disease. We showed that stimulation of locus coeruleus by 1-dopa induces bladder overactivity and suppressed by tachykinin receptor antagonists, and also the lack of dopamine 1 receptor antagonist may play a role of overactive bladder in Parkinson's disease.By aging, the nervous control of micturition changes and the mechanism cannot be explained by only adrenergic and parasympathetic nervous control. 5-HT receptors are widely distributed in the central nervous system, including several areas involved in the-control of micturition reflex pathways. We showed that 5-HT receptor antagonists,-acting at 5-HT1A, 5-HT2 and 5-HT4 receptors, could be targets for drugs meant for treatment of bladder hyperactivity.

我们采用多种疾病大鼠模型研究了中枢性膀胱功能亢进，膀胱出口梗阻，如前列腺增生症，是引起膀胱功能亢进的常见疾病。这种多动可能是由于中枢神经对排尿的控制障碍所致。本研究表明，在脊髓上水平，速激肽和α1肾上腺素能受体也可能参与排尿控制，尤其是在膀胱出口梗阻大鼠。结果提示脊髓上NK受体和肾上腺素能受体可能是治疗膀胱出口梗阻后膀胱过度活动的药物作用靶点，脑桥蓝斑是诱发帕金森病症状的重要部位之一。我们发现，1-多巴刺激蓝斑可引起膀胱过度活动，并被速激肽受体拮抗剂抑制，多巴胺1受体拮抗剂的缺乏可能在帕金森病的膀胱过度活动中起作用，随着年龄的增长，排尿的神经控制发生变化，其机制不能仅用肾上腺素能和副交感神经控制来解释。5-HT受体广泛分布于中枢神经系统，包括参与排尿反射通路控制的几个区域。我们发现，5-HT受体拮抗剂，作用于5-HT 1A，5-HT 2和5-HT 4受体，可以作为治疗膀胱过度活动的药物的靶点。