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Overactive bladder--experimental aspects
Osamu Yokoyama1, Kazuto Komatsu, Yoshiyuki Ishiura
1Department of Urology, Kanazawa University School of Medicine, Japan. oyoko@fmsrsa.fukui-med.ac.jp
Scandinavian Journal of Urology and Nephrology. Supplementum
|December 12, 2002
Summary
Neurological disorders affecting the brainstem's micturition center can cause bladder overactivity. This is linked to changes in neurotransmitter systems, impacting bladder control.
Area of Science:
- Neuroscience
- Urology
- Neurology
Background:
- Supra-pontine lesions from neurological disorders disrupt cortical control over the pontine micturition center (PMC).
- This disruption involves alterations in neurotransmitter systems like glutamate, dopamine, GABA, and acetylcholine.
- These changes lead to increased bladder activity, commonly known as bladder overactivity.
Purpose of the Study:
- To elucidate the neurochemical mechanisms underlying bladder overactivity in supra-pontine lesions.
- To investigate the roles of specific neurotransmitter systems in bladder dysfunction associated with vascular disease, Parkinson's disease, and Alzheimer's disease.
Main Methods:
- Analysis of neurotransmitter system involvement in bladder overactivity.
- Examination of molecular changes, including mRNA expression (c-fos, zif268, COX-2), in the dorsal pontine tegmentum following cerebral infarction.
Main Results:
- Cerebral infarction-induced bladder overactivity involves NMDA glutamatergic and D2 dopaminergic upregulation, and NMDA glutamatergic and M1 muscarinic downregulation.
- Parkinson's disease-related bladder overactivity may stem from reduced D1 dopaminergic receptor input.
- Alzheimer's disease-related bladder overactivity is associated with M1 muscarinic inhibitory mechanism downregulation.
- Cerebral infarction leads to NMDA receptor activation and increased c-fos, zif268, and COX-2 mRNA in the dorsal pontine tegmentum.
Conclusions:
- Supra-pontine lesions significantly alter brainstem pathways controlling micturition.
- Neurotransmitter dysregulation, particularly involving glutamate and dopamine, is a key factor in neurological bladder overactivity.
- Understanding these mechanisms is crucial for developing targeted therapies for bladder dysfunction in neurodegenerative and cerebrovascular diseases.