Parkinson’s disease is a progressive neurodegenerative disorder in which gastrointestinal and urinary disturbances commonly occur alongside motor symptoms, suggesting a possible role of the peripheral autonomic nervous system in disease pathophysiology.
In this Master’s thesis, we investigated whether systemic peripheral catecholaminergic injury induced by 6-hydroxydopamine (6-OHDA) causes structural and functional changes in the distal colon and urinary bladder. The effectiveness of the model was assessed by tyrosine hydroxylase immunohistochemistry.
The expression of selected markers was evaluated by immunofluorescence staining, while functional changes were investigated using organ bath experiments.
Systemic 6-OHDA administration caused a marked reduction in tyrosine hydroxylase immunoreactivity in cardiac tissue, whereas no obvious lesions were observed in the striatum or substantia nigra, supporting the predominantly peripheral nature of the model.
No statistically significant differences in the expression of the analysed markers were observed between the groups in either the distal colon or urinary bladder. Likewise, no significant differences in functional responses were detected in the urinary bladder.
In contrast, in distal colon contractions induced by electrical field stimulation were significantly reduced, while reduced responses were also observed following methacholine and serotonin stimulation. Noradrenaline-induced relaxation was significantly smaller in 6-OHDA-treated animals.
These findings indicate that peripheral catecholaminergic injury produces persistent functional changes predominantly in the distal colon, whereas the urinary bladder appears to be less markedly affected in this model.
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