ArticlePloS one2014
Alterations in nerve-evoked bladder contractions in a coronavirus-induced mouse model of multiple sclerosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Comparative transcriptome profiling of the lumbosacral dorsal root ganglia reveals sexually dimorphic gene expression in a murine model of coronavirus-induced neurodegeneration.American journal of clinical and experimental urology · 2025Article
- Differential transcriptomic changes in the central nervous system and urinary bladders of mice infected with a coronavirus.PloS one · 2022Article
- PART 2: Mouse models for multiple sclerosis research.Neurourology and urodynamics · 2021Review
- Increased expression of desmin and vimentin reduces bladder smooth muscle contractility via JNK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Potential of SARS-CoV-2 to Cause CNS Infection: Biologic Fundamental and Clinical Experience.Frontiers in neurology · 2020Review
- Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.Scientific reports · 2019Article
- New Frontiers of Basic Science Research in Neurogenic Lower Urinary Tract Dysfunction.The Urologic clinics of North America · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPatients with neurodegenerative diseases such as multiple sclerosis, Parkinson's, and Alzheimer's often present with lower urinary tract symptoms (LUTS, urinary frequency, urgency, nocturia and retention) resulting from damage to the peripheral and central nervous systems. These studies were designed to examine the changes in the function of the bladder that may underlie neurogenic bladder dysfunction using a mouse model of demyelination in the CNS.
methodsBladders from 12 week old male C57BL/6J mice with coronavirus-induced encephalomyelitis (CIE, a chronic, progressive demyelinating disease model of human MS), and age-matched controls, were cut into 5-7 strips and suspended in physiological muscle baths for tension measurement in response to agonists and electric field stimulation (EFS). Experiments were performed on intact and denuded (with mucosa removed) bladder strips.
resultsThe maximum effect of EFS was not significantly different between CIE and control bladders. Nerve-evoked EFS contractions (tetrodotoxin-sensitive) were blocked by a combination of atropine (cholinergic antagonist) and α,β-methylene ATP (an ATP analog that desensitizes purinergic receptors). In response to EFS, the α,β-methylene ATP-resistant (cholinergic) component of contraction was significantly reduced, while the atropine-resistant (purinergic) component was significantly increased in CIE bladders. Removal of the mucosa in CIE bladders restored the cholinergic component. Bethanechol (muscarinic receptor agonist) potency was significantly increased in CIE bladders.
conclusionsOur data demonstrate a deficit in the nerve-evoked cholinergic component of contraction that is not due to the ability of the smooth muscle to respond to acetylcholine. We conclude that neurodegenerative bladder dysfunction in this model of multiple sclerosis may be due, in part, to pathologic changes in the mucosa that causes suppression of muscarinic receptor-mediated contractile response and augmentation of purinergic response of the underlying muscle. Further studies utilizing CIE mice should help elucidate the pathological changes in the mucosa resulting from demyelination in the CNS.
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