ArticleNPJ Parkinson's disease2019
Contractile dysfunction and nitrergic dysregulation in small intestine of a primate model of Parkinson's disease.
Article in NPJ Parkinson's disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Gastrointestinal Issues in Depression, Anxiety, and Neurodegenerative Diseases: A Systematic Review on Pathways and Clinical Targets Implications.CNS & neurological disorders drug targets · 2024Pooled it
- Mechanics of small intestine motility for oral macromolecular delivery: modelling segmentation versus peristalsis.Drug delivery · 2026Article
- Prolactin and oxytocin as modulators of intestinal contractility and glucose uptake.Frontiers in physiology · 2026Article
- From the Gut to the Brain: The Role of Enteric Glial Cells and Their Involvement in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- 6-OHDA-Induced Changes in Colonic Segment Contractility in the Rat Model of Parkinson's Disease.Gastroenterology research and practice · 2023Article
- Ganoderma lucidum polysaccharide ameliorated diabetes mellitus-induced erectile dysfunction in rats by regulating fibrosis and the NOS/ERK/JNK pathway.Translational andrology and urology · 2022Article
- Gastrointestinal dysfunction in the synucleinopathies.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021Review
- Characterization of Gastrointestinal Symptom Type and Severity in Parkinson's Disease: A Case-Control Study in an Australian Cohort.Movement disorders clinical practice · 2021Article
- Dysregulation of epithelial ion transport and neurochemical changes in the colon of a parkinsonian primate.NPJ Parkinson's disease · 2021Article
- Myorelaxant and antispasmodic effect of an aqueous extract of Artemisia campestris L. via calcium channel blocking and anticholinergic pathways.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2021Article
- Gastrointestinal and metabolic function in the MPTP-treated macaque model of Parkinson's disease.Heliyon · 2020Article
- Cerebral dopamine neurotrophic factor is essential for enteric neuronal development, maintenance, and regulation of gastrointestinal transit.The Journal of comparative neurology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bowel dysfunction is a common non-motor symptom in Parkinson's disease (PD). The main contractile neurotransmitter in the GI tract is acetylcholine (ACh), while nitric oxide (NO) causes the relaxation of smooth muscle in addition to modulating ACh release. The aim of this study was to characterise functional and neurochemical changes in the isolated ileum of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated marmoset, an established model of PD motor dysfunction. While NO-synthase inhibitor L-NAME concentration dependently augmented the neurogenically-evoked contractions and inhibited the relaxations in normal tissues, it had no effects on the MPTP ileum. Immunohistochemical analyses of the myenteric plexus showed that ChAT-immunoreactivity (-ir) was significantly reduced and the density of the enteric glial cells as shown by SOX-10-ir was increased. However, no change in TH-, 5-HT-, VIP- or nNOS-ir was observed in the MPTP tissues. The enhancement of the neurogenically-evoked contractions and the inhibition of the relaxation phase by L-NAME in the control tissues is in line with NO's direct relaxing effect on smooth muscle and its indirect inhibitory effect on ACh release. The absence of the relaxation and the inefficacy of L-NAME in the MPTP tissues suggests that central dopaminergic loss dopamine may eventually lead to the impairment of NO signal coupling that affects bowel function, and this may be the result of a complex dysregulation at the level of the neuroeffector junction.
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