Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 114, Issue 18, Pages E3709-E3718Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1619406114
Keywords
enteric neurons; adult neurogenesis; Nestin; enteric neural precursor cells; neuronal apoptosis
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases [R01DK080920, P30 DK089502]
- NIH [OT2-OD023849, R01GM114254, R01DE022750, R01GM087369]
- Defense Advanced Research Planning Agency [N660015-2-4059]
- Johns Hopkins University Brain Science Institute
- Howard Hughes Medical Institute
- Kenneth Rainin Foundation
- National Institute of Allergy and Infectious Diseases [R21 AI126351 01]
- March of Dimes [1FY-12-450]
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According to current dogma, there is little or no ongoing neurogenesis in the fully developed adult enteric nervous system. This lack of neurogenesis leaves unanswered the question of how enteric neuronal populations are maintained in adult guts, given previous reports of ongoing neuronal death. Here, we confirm that despite ongoing neuronal cell loss because of apoptosis in the myenteric ganglia of the adult small intestine, total myenteric neuronal numbers remain constant. This observed neuronal homeostasis is maintained by new neurons formed in vivo from dividing precursor cells that are located within myenteric ganglia and express both Nestin and p75NTR, but not the pan-glial marker Sox10. Mutation of the phosphatase and tensin homolog gene in this pool of adult precursors leads to an increase in enteric neuronal number, resulting in ganglioneuromatosis, modeling the corresponding disorder in humans. Taken together, our results show significant turnover and neurogenesis of adult enteric neurons and provide a paradigm for understanding the enteric nervous system in health and disease.
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