The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease

Abstract Parkinson’s disease (PD) is associated with neuronal damage in the brain and gut. This work compares changes in the enteric nervous system (ENS) of commonly used mouse models of PD that exhibit central neuropathy and a gut phenotype. Enteric neuropathy was assessed in five mouse models: per...

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Autores principales:	Rachel M. McQuade, Lewis M. Singleton, Hongyi Wu, Sophie Lee, Remy Constable, Madeleine Di Natale, Mitchell T. Ringuet, Joel P. Berger, Jessica Kauhausen, Clare L. Parish, David I. Finkelstein, John B. Furness, Shanti Diwakarla
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/84b393003cc04c729aedad1290f826e6
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spelling	oai:doaj.org-article:84b393003cc04c729aedad1290f826e62021-12-02T18:02:57ZThe association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease10.1038/s41598-021-86917-52045-2322https://doaj.org/article/84b393003cc04c729aedad1290f826e62021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-86917-5https://doaj.org/toc/2045-2322Abstract Parkinson’s disease (PD) is associated with neuronal damage in the brain and gut. This work compares changes in the enteric nervous system (ENS) of commonly used mouse models of PD that exhibit central neuropathy and a gut phenotype. Enteric neuropathy was assessed in five mouse models: peripheral injection of MPTP; intracerebral injection of 6-OHDA; oral rotenone; and mice transgenic for A53T variant human α-synuclein with and without rotenone. Changes in the ENS of the colon were quantified using pan-neuronal marker, Hu, and neuronal nitric oxide synthase (nNOS) and were correlated with GI function. MPTP had no effect on the number of Hu+ neurons but was associated with an increase in Hu+ nuclear translocation (P < 0.04). 6-OHDA lesioned mice had significantly fewer Hu+ neurons/ganglion (P < 0.02) and a reduced proportion of nNOS+ neurons in colon (P < 0.001). A53T mice had significantly fewer Hu+ neurons/area (P < 0.001) and exhibited larger soma size (P < 0.03). Treatment with rotenone reduced the number of Hu+ cells/mm2 in WT mice (P < 0.006) and increased the proportion of Hu+ translocated cells in both WT (P < 0.02) and A53T mice (P < 0.04). All PD models exhibited a degree of enteric neuropathy, the extent and type of damage to the ENS, however, was dependent on the model.Rachel M. McQuadeLewis M. SingletonHongyi WuSophie LeeRemy ConstableMadeleine Di NataleMitchell T. RinguetJoel P. BergerJessica KauhausenClare L. ParishDavid I. FinkelsteinJohn B. FurnessShanti DiwakarlaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rachel M. McQuade Lewis M. Singleton Hongyi Wu Sophie Lee Remy Constable Madeleine Di Natale Mitchell T. Ringuet Joel P. Berger Jessica Kauhausen Clare L. Parish David I. Finkelstein John B. Furness Shanti Diwakarla The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
description	Abstract Parkinson’s disease (PD) is associated with neuronal damage in the brain and gut. This work compares changes in the enteric nervous system (ENS) of commonly used mouse models of PD that exhibit central neuropathy and a gut phenotype. Enteric neuropathy was assessed in five mouse models: peripheral injection of MPTP; intracerebral injection of 6-OHDA; oral rotenone; and mice transgenic for A53T variant human α-synuclein with and without rotenone. Changes in the ENS of the colon were quantified using pan-neuronal marker, Hu, and neuronal nitric oxide synthase (nNOS) and were correlated with GI function. MPTP had no effect on the number of Hu+ neurons but was associated with an increase in Hu+ nuclear translocation (P < 0.04). 6-OHDA lesioned mice had significantly fewer Hu+ neurons/ganglion (P < 0.02) and a reduced proportion of nNOS+ neurons in colon (P < 0.001). A53T mice had significantly fewer Hu+ neurons/area (P < 0.001) and exhibited larger soma size (P < 0.03). Treatment with rotenone reduced the number of Hu+ cells/mm2 in WT mice (P < 0.006) and increased the proportion of Hu+ translocated cells in both WT (P < 0.02) and A53T mice (P < 0.04). All PD models exhibited a degree of enteric neuropathy, the extent and type of damage to the ENS, however, was dependent on the model.
format	article
author	Rachel M. McQuade Lewis M. Singleton Hongyi Wu Sophie Lee Remy Constable Madeleine Di Natale Mitchell T. Ringuet Joel P. Berger Jessica Kauhausen Clare L. Parish David I. Finkelstein John B. Furness Shanti Diwakarla
author_facet	Rachel M. McQuade Lewis M. Singleton Hongyi Wu Sophie Lee Remy Constable Madeleine Di Natale Mitchell T. Ringuet Joel P. Berger Jessica Kauhausen Clare L. Parish David I. Finkelstein John B. Furness Shanti Diwakarla
author_sort	Rachel M. McQuade
title	The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
title_short	The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
title_full	The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
title_fullStr	The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
title_full_unstemmed	The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease
title_sort	association of enteric neuropathy with gut phenotypes in acute and progressive models of parkinson’s disease
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/84b393003cc04c729aedad1290f826e6
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The association of enteric neuropathy with gut phenotypes in acute and progressive models of Parkinson’s disease

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