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dc.creatorFrara, Nagat
dc.date.accessioned2023-06-06T19:58:33Z
dc.date.available2023-06-06T19:58:33Z
dc.date.issued2022-10-01
dc.identifier.urihttp://hdl.handle.net/20.500.12613/8686
dc.descriptionSupplemental Figures and Figure legends for: Nerve transfer for restoration of lower motor neuron-lesioned bladder, urethral and anal sphincter function in a dog model. Part 3: Neuropharmacological characterization of nicotinic receptors in vitro.
dc.description.abstractVery little is known about the physiological role of nicotinic receptors in canine bladders, although functional nicotinic receptors have been reported in bladders of many species. Utilizing in vitro methods, we evaluated nicotinic receptors mediating bladder function in dogs: Control (9 female and 11 male normal controls, 5 sham-operated), Decentralized (9 females, decentralized 6-21 mo), and obturator-to-pelvic nerve transfer reinnervated (ObNT-Reinn; 9 females; decentralized 9-13 mo, then reinnervated with 8-12 mo recovery). Muscle strips were collected, mucosa-denuded and mounted in muscle baths before incubation with neurotransmitter antagonists and contractions to the nicotinic receptor agonist epibatidine was determined. Strip response to epibatidine, expressed as percent potassium chloride, were similar (approximately 35% in Controls, 30% in Decentralized, and 24% in ObNT-Reinn). Differentially, epibatidine responses in Decentralized and ObNT-Reinn bladder strips were lower than Controls after tetrodotoxin (a sodium channel blocker that inhibits axonal action potentials). Yet, in all groups, epibatidine-induced strip contractions were similarly inhibited by mecamylamine and hexamethonium (ganglionic nicotinic receptor antagonists), SR 16584 (α3β4 neuronal nicotinic receptor antagonist), atracurium and tubocurarine (neuromuscular nicotinic receptor antagonists), and atropine (muscarinic receptor antagonist), indicating that nicotinic receptors (particularly α3β4 subtypes), neuromuscular and muscarinic receptors play roles in bladder contractility. In Control bladder strips, since tetrodotoxin did not inhibit epibatidine contractions, nicotinic receptors are likely located on nerve terminals. The tetrodotoxin inhibition of epibatidine-induced contractions in Decentralized and ObNT-Reinn suggests a relocation of nicotinic receptors from nerve terminals to more distant axonal sites, perhaps as a compensatory mechanism to recover bladder function.
dc.format.extent11 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.rightsAll Rights Reserved
dc.titleSupplemental Figures S1-S11_for AJP_6-6-2023
dc.typeText
dc.type.genreFigure
dc.contributor.groupCenter for Translational Medicine (Temple University)
dc.relation.doihttp://dx.doi.org/10.34944/dspace/8650
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeLewis Katz School of Medicine
dc.temple.creatorFrara, Nagat
refterms.dateFOA2023-06-06T19:58:33Z


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