Abstract
Neurotransmitters are special molecules that serve as messengers in chemical synapses between neurons, cells, or receptors, including catecholamines, serotonin, dopamine, and other neurotransmitters, which play an important role in both human physiology and pathology. Compelling evidence has indicated that neurotransmitters have an important physiological role in various digestive diseases. They act as ligands in combination with central or peripheral receptors, and transmits signals through chemical synapses, which are involved in regulating the physiological and pathological processes of the digestive tract organs. For instance, neurotransmitters regulate blood circulation and affect intestinal movement, nutrient absorption, the gastrointestinal innate immune system, and the microbiome. In this review, we will focus on the role of neurotransmitters in the pathogenesis of digestive tract diseases to provide novel therapeutic targets for new drug development in digestive diseases.
Highlights
Neurotransmitters are hormonal factors, but are a cell signaling factors
The imbalance of neurotransmitter release, excessive activation of receptors, or loss of their function is closely related to the pathological state of digestive tract organs. 5-HT and its receptors are mainly distributed in smooth muscle cells, so 5-HT signaling is very important for the motility balance of the esophagus and gastrointestinal tract
Animal experiments found that the administration of receptor blockers aggravated gastrointestinal inflammation, which seemed to suggest that 5-HT signaling is involved in the defense of gastrointestinal inflammation
Summary
Neurotransmitters are hormonal factors, but are a cell signaling factors. In the human HCC cell line Huh7, serotonin stimulates proliferation in serum deprived medium via upregulation and phosphorylation of forkhead transcription factor o subfamily member 3a (FOXO3a), and this effect involved in the 5-HT receptor 2B (5-HT2B) (Liang et al, 2013). Ganguly et al (2010) found that dopamine inhibits insulin-like growth factor-I induced gastric cancer cell proliferation for upregulation of insulin-like growth factor-I receptor via activation of D2 receptors.
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