scholarly journals Delayed gastric emptying and enteric nervous system dysfunction in the rotenone model of Parkinson's disease

2009 ◽  
Vol 218 (1) ◽  
pp. 154-161 ◽  
Author(s):  
James G. Greene ◽  
Ali Reza Noorian ◽  
Shanthi Srinivasan
Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 732
Author(s):  
Gianfranco Natale ◽  
Larisa Ryskalin ◽  
Gabriele Morucci ◽  
Gloria Lazzeri ◽  
Alessandro Frati ◽  
...  

The gastrointestinal (GI) tract is provided with a peculiar nervous network, known as the enteric nervous system (ENS), which is dedicated to the fine control of digestive functions. This forms a complex network, which includes several types of neurons, as well as glial cells. Despite extensive studies, a comprehensive classification of these neurons is still lacking. The complexity of ENS is magnified by a multiple control of the central nervous system, and bidirectional communication between various central nervous areas and the gut occurs. This lends substance to the complexity of the microbiota–gut–brain axis, which represents the network governing homeostasis through nervous, endocrine, immune, and metabolic pathways. The present manuscript is dedicated to identifying various neuronal cytotypes belonging to ENS in baseline conditions. The second part of the study provides evidence on how these very same neurons are altered during Parkinson’s disease. In fact, although being defined as a movement disorder, Parkinson’s disease features a number of degenerative alterations, which often anticipate motor symptoms. Among these, the GI tract is often involved, and for this reason, it is important to assess its normal and pathological structure. A deeper knowledge of the ENS is expected to improve the understanding of diagnosis and treatment of Parkinson’s disease.


2010 ◽  
Vol 258 (3) ◽  
pp. 421-426 ◽  
Author(s):  
Yuji Tanaka ◽  
Tomohiro Kato ◽  
Hiroshi Nishida ◽  
Megumi Yamada ◽  
Akihiro Koumura ◽  
...  

2013 ◽  
Vol 29 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Sarah Marrinan ◽  
Anton V. Emmanuel ◽  
David J. Burn

2019 ◽  
Vol 32 (1) ◽  
Author(s):  
Sarah M. O’Donovan ◽  
Erin K. Crowley ◽  
Jillian R.‐M. Brown ◽  
Orla O’Sullivan ◽  
Olivia F. O’Leary ◽  
...  

Brain ◽  
2020 ◽  
Vol 143 (5) ◽  
pp. 1462-1475 ◽  
Author(s):  
Marie-Laure Arotcarena ◽  
Sandra Dovero ◽  
Alice Prigent ◽  
Mathieu Bourdenx ◽  
Sandrine Camus ◽  
...  

Abstract In Parkinson’s disease, synucleinopathy is hypothesized to spread from the enteric nervous system, via the vagus nerve, to the CNS. Here, we compare, in baboon monkeys, the pathological consequences of either intrastriatal or enteric injection of α-synuclein-containing Lewy body extracts from patients with Parkinson’s disease. This study shows that patient-derived α-synuclein aggregates are able to induce nigrostriatal lesions and enteric nervous system pathology after either enteric or striatal injection in a non-human primate model. This finding suggests that the progression of α-synuclein pathology might be either caudo-rostral or rostro-caudal, varying between patients and disease subtypes. In addition, we report that α-synuclein pathological lesions were not found in the vagal nerve in our experimental setting. This study does not support the hypothesis of a transmission of α-synuclein pathology through the vagus nerve and the dorsal motor nucleus of the vagus. Instead, our results suggest a possible systemic mechanism in which the general circulation would act as a route for long-distance bidirectional transmission of endogenous α-synuclein between the enteric and the central nervous systems. Taken together, our study provides invaluable primate data exploring the role of the gut-brain axis in the initiation and propagation of Parkinson’s disease pathology and should open the door to the development and testing of new therapeutic approaches aimed at interfering with the development of sporadic Parkinson’s disease.


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