Study of neuroplastic centrally induced bladder hyper activity and gene therapy

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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.