Aging of the myenteric plexus: neuronal loss is specific to cholinergic neurons

2003 ◽  
Vol 106 (2) ◽  
pp. 69-83 ◽  
Author(s):  
Robert J Phillips ◽  
Elizabeth J Kieffer ◽  
Terry L Powley
2014 ◽  
Vol 60 (4) ◽  
pp. 841-849 ◽  
Author(s):  
Evandro José Beraldi ◽  
Angélica Soares ◽  
Stephanie Carvalho Borges ◽  
Aline Cristine da Silva de Souza ◽  
Maria Raquel Marçal Natali ◽  
...  

2020 ◽  
Vol 9 (1) ◽  
pp. 14
Author(s):  
Ricardo De Melo Germano ◽  
Renata De Britto Mari ◽  
Paula Montanhini Favetta ◽  
Marcelo Alberto Elias ◽  
Wesley Alves Trindade ◽  
...  

The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) is widely used in several countries. Research on the neurotoxicity of 2,4-D has been focused on the central nervous system, and little is known about its effects on the myenteric plexus. Therefore, to elucidate the neurotoxicity of 2,4-D and the viability of its use, we investigated the effects of daily intake of 5 mg 2,4-D/kg for 60 days on the myenteric plexus neurons of the rat ileum using quantitative and morphometric analyses. Twenty male Wistar rats aged 60 days were divided into two groups (n=10 rats/group). The group E animals received daily 5 mg doses of 2,4-D/kg diluted in 1 mL of water, whereas the group C animals were not treated with the herbicide. The animals were euthanized with anesthetic after 60 days; subsequently, the ileum was dissected out, and procedures were performed to visualize the total population of neurons (Giemsa staining), the nitrergic neurons (NADPHd+), and the estimated population of cholinergic neurons (NADPHd-). The results were statistically analyzed and compared between groups. In group E, the densities of Giemsa-stained neurons and NADPHd- neurons decreased (p<0.05) by 7% and 10%, respectively, whereas the density of NADPHd+ neurons remained constant. The cell body area was 5.8% greater (p<0.05) for the NADPHd+ neurons but remained unchanged for the neurons stained with Giemsa. These results suggest that 2,4-D causes a reduction in neuronal density, particularly for cholinergic neurons, and promotes an increase in the cell body area of nitrergic neurons, leading to hypertrophy.


Author(s):  
R Chiocchetti ◽  
T Hitrec ◽  
F Giancola ◽  
J Sadeghinezhad ◽  
F Squarcio ◽  
...  

AbstractTau protein is of primary importance for neuronal homeostasis and when hyperphosphorylated (PP-Tau), it tends to aggregate in neurofibrillary tangles, as is the case with tauopathies, a class of neurodegenerative disorders. Reversible PP-Tau accumulation occurs in the brain of hibernating rodents and it was recently observed in rats (a non-hibernator) during synthetic torpor (ST), a pharmacological-induced torpor-like condition. To date, the expression of PP-Tau in the rat enteric nervous system (ENS) is still unknown. The present study immunohistochemically investigates the PP-Tau expression in the myenteric plexus of the ileum and colon of normothermic rats (CTRL) and during ST, focusing on the two major subclasses of enteric neurons, i.e., cholinergic and nitrergic.Results showed that both groups of rats expressed PP-Tau, with a significantly increased percentage of PP-Tau immunoreactive (IR) neurons in ST vs. CTRL. In all rats, the majority of PP-Tau-IR neurons were cholinergic. In ST rats, the percentage of PP-Tau-IR neurons expressing a nitrergic phenotype increased, although with no significant differences between groups. In addition, the ileum of ST rats showed a significant decrease in the percentage of nitrergic neurons. In conclusion, our findings suggest an adaptive response of ENS to very low core body temperatures, with changes involving PP-tau expression in enteric neurons, especially the ileal nitrergic subpopulation. In addition, the high presence of PP-Tau in cholinergic neurons, specifically, is very interesting and deserves further investigation. Altogether, these data strengthen the hypothesis of a common cellular mechanism triggered by ST, natural hibernation and tauopathies occurring in ENS neurons.


Author(s):  
Lucas D. Udovin ◽  
Andrea Aguilar ◽  
Tamara Kobiec ◽  
María I. Herrera ◽  
Santiago Perez Lloret ◽  
...  

Progressive neuronal loss is a typical characteristic of neurodegenerative diseases. In Parkinson’s disease, the loss of dopaminergic neurons in the basal ganglia results in impaired mobility and flawed muscle control. The loss of cholinergic neurons largely in the basal forebrain contributes to memory and attention deficits and the overall cognitive impairment in Alzheimer’s disease. This being said, neuroprotective drugs should be expected to preserve and/or restore the functions affected by neuronal loss, and substantially prevent cell death. The endocannabinoid system, comprising lipid mediators able to bind to and activate cannabinoid receptors, has emerged as a therapeutic target of potential interest in a variety of central nervous system diseases. Palmitoylethanolamide (PEA) is one of the most important endocannabinoids, which has a key role in modulating oxidative stress and inflammatory response with neuroprotective potential in neurological disorders. Neurodegenerative diseases undergo varied, progressive stages. The current therapeutical approaches are beginning to fall short when it comes to meet the expected results, urging to either develop or identify or develop new effective treatments. This chapter discusses the neuroprotective potential of new drugs, aiming to shed some light on their proposed mechanism of action and their effect in cellular and animal models of neurodegeneration.


2011 ◽  
Vol 164 (1-2) ◽  
pp. 51-61 ◽  
Author(s):  
Stella M. Honoré ◽  
Laura C. Zelarayan ◽  
Susana B. Genta ◽  
Sara S. Sánchez

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