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Altered detrusor contractility in MPTP-treated common marmosets with bladder hyperreflexia
Sara Pritchard1, Michael J Jackson2, Atsuko Hikima2
1Department of Pharmacy, Pharmacology and Postgraduate Medicine, University of Hertfordshire, Hatfield, United Kingdom.
Plos One
|May 19, 2017
Summary
Parkinson's disease causes bladder hyperreflexia. MPTP-treated marmoset detrusor muscle showed increased spontaneous contractions and enhanced neurogenic responses, suggesting local adaptive changes due to dopamine pathway loss.
Area of Science:
- Neuroscience
- Urology
- Pharmacology
Background:
- Bladder hyperreflexia is a frequent non-motor symptom in Parkinson's disease.
- The underlying mechanisms, particularly in the detrusor muscle, are not fully understood.
Purpose of the Study:
- To investigate the contractility of isolated primate detrusor smooth muscle.
- To determine the effects of MPTP-induced Parkinsonism on detrusor muscle contractility and neurogenic responses.
Main Methods:
- Isolated detrusor smooth muscle strips from normal and MPTP-treated common marmosets (Callithrix jacchus) were studied.
- Spontaneous and evoked (carbachol, histamine, ATP, electrical field stimulation [EFS]) contractions were measured.
- Responses to receptor agonists and antagonists were assessed.
Main Results:
- MPTP treatment increased spontaneous detrusor contractions.
- Neurogenic contractions evoked by EFS were significantly greater in MPTP-treated animals.
- Non-cholinergic neurogenic contractions were enhanced, suggesting a preferential increase in non-cholinergic transmission.
Conclusions:
- The study indicates that MPTP-induced Parkinsonism alters primate detrusor contractility.
- Enhanced neurogenic contractions, particularly non-cholinergic, may contribute to bladder hyperreflexia.
- These changes might result from local adaptive mechanisms following nigrostriatal pathway degeneration.

