Gastrointestinal autonomic nerve tumors (GANTs) are rare tumors, probably developing from the
myenteric plexus of Auerbach.
During embryologic development, submucosal ganglion cells form from the descendants of progenitors located in the
myenteric plexus, which migrate centrifugally toward the bowel lumen.
In achalasia patients, studies suggested that loss of NO-secreting esophageal
myenteric plexus neurons caused imbalance of excitatory and inhibitory neurons, leading to altered manometry results.[4] We detected iNOS and nNOS mRNA in both achalasia and control tissues as positive, but only nNOS was positive in IHC.
The
myenteric plexus is situated between the circular and longitudinal muscle layers and influences GI motility.
The histological growth pattern varies from fusiform, hyperplastic expansions of the
myenteric plexus to confluent, irregular, transmural ganglioneuromatous proliferations that distort the
myenteric plexus and infiltrates the adjacent bowel wall.
Another nerve plexus, the
myenteric plexus (Auerbach's plexus), is present between the outer and inner muscle layers.
[6] The ENS is composed of an inner plexus known as Meissner's or submucosal plexus located in the submucosal layer, mainly implicated in regulation of secretion, and an outer plexus known as Auerbach's or
myenteric plexus located between the intestinal muscular layers and involved in regulation of smooth muscle contractility.
It originates from the nerve sheath of
myenteric plexus or less commonly from meissner plexus, with gradual increase in the size of the tumor compression symptoms appear6.
In achalasia, the absent or diminished relaxation of the lower oesophageal sphincter and absent peristalsis of the tubular oesophagus in response to swallowing are thought to be because of the loss of inhibitory nitrinergic neurons in the oesophageal
myenteric plexus. The cause of this loss is unclear, and genetic, autoimmune or infectious origins of neuronal damage have been suggested.
The purpose of this study was to investigate the effects of the quercetin supplementation in NADH-d neuronal subpopulation in the ileum of rats with experimental diabetes, since the pathophysiological conditions present in the diabetes could be generated by the reduction in the levels of antioxidant defense and consequent increase in the oxidative stress, among other factors that may compromise the function of neurons in the
myenteric plexus.