Abstract
Nitrergic enteric neurons are key players of the descending inhibitory reflex of intestinal peristalsis, therefore loss or damage of these neurons can contribute to developing gastrointestinal motility disturbances suffered by patients worldwide. There is accumulating evidence that the vulnerability of nitrergic enteric neurons to neuropathy is strictly region-specific and that the two main enteric plexuses display different nitrergic neuronal damage. Alterations both in the proportion of the nitrergic subpopulation and in the total number of enteric neurons suggest that modification of the neurochemical character or neuronal death occurs in the investigated gut segments. This review aims to summarize the gastrointestinal region and/or plexus-dependent pathological changes in the number of nitric oxide synthase (NOS)-containing neurons, the NO release and the cellular and subcellular expression of different NOS isoforms. Additionally, some of the underlying mechanisms associated with the nitrergic pathway in the background of different diseases, e.g., type 1 diabetes, chronic alcoholism, intestinal inflammation or ischaemia, will be discussed.
Highlights
In the gastrointestinal (GI) tract, as in most other organ systems, nitric oxide (NO) plays a defining role in regulating several functions in both physiological and pathological states
It is well established that nitric oxide synthase (NOS)-containing myenteric neurons are curiously susceptible to diabetic injuries [26,27,28] and impaired nitrergic innervation is accompanied by motility dysfunction
It is well established that NOS-containing myenteric neurons are curiously susceptible to diabetic injuries [26,27,28] and impaired nitrergic innervation is accompanied by motility dysfunction [29]
Summary
In the gastrointestinal (GI) tract, as in most other organ systems, nitric oxide (NO) plays a defining role in regulating several functions in both physiological and pathological states. NO contributes to the maintenance of GI mucosal integrity and circulation, regulation of secretion, smooth muscle function or mucosal inflammation [1,2]. NO, produced by neuronal NO synthase (nNOS), is one of the main inhibitory neurotransmitters in GI smooth muscle [3,4]. The involvement of nNOS and NO pathways in enteric neuropathies was well-described in a variety of disorders, like esophageal or internal anal sphincter achalasia, hypertrophic pyloric stenosis, gastroparesis, Chagas’, or Hirschsprung’s disease [5]. This review will provide information about the role of enteric neuronal NO in health and different pathological animal models with type 1 diabetes, chronic alcoholism, intestinal inflammation, or ischaemia
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