Highlights
- •Dopamine (DA) is a catecholamine neurotransmitter with potential role in physiology/physiopathology of the intestinal tract.
- •DA is able to modulate intestinal functions via activation of peripherally located receptors, classified in two main classes, D1-like and D2-like receptors.
- •DA receptor activation induces mainly inhibitory effects on the intestinal contractility, in animal models and in humans.
- •DA plays an important role in the protection of the gastrointestinal mucosal barrier.
- •Decreased DA level upon the onset of intestinal inflammation, would favour the development of colitis.
Abstract
Dopamine (DA) is a catecholamine regulatory molecule with potential role in physiology
and physiopathology of the intestinal tract. Various cellular sources of DA have been
indicated as enteric neurons, immune cells, intestinal flora and gastrointestinal
epithelium. Moreover, DA is produced by nutritional tyrosine. All the five DA receptors,
actually described, are present throughout the gut. Current knowledge of DA in this
area is reviewed, focusing on gastrointestinal function in health and during inflammation.
Research on animal models and humans are reported. A major obstacle to understanding
the physiologic and/or pharmacological roles of enteric DA is represented by the multiplicity
of receptors involved in the responses together with many signalling pathways related
to each receptor subtype. It is mandatory to map precisely the distributions of DA
receptors, to determine the relevance of a receptor in a specific location in order
to explore novel therapies directed to dopaminergic targets that may be useful in
the control of intestinal inflammation.
Graphical abstract

Graphical Abstract
Abbreviations:
DA (dopamine), DAT (dopamine transporter), D1-D5 (dopamine receptors), GI (gastrointestinal), IBD (inflammatory bowel diseases), L-DOPA (L-3,4-dihydroxyphenylalanine), TH (tyrosine hydroxylase)Keywords
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Article info
Publication history
Published online: November 07, 2022
Accepted:
November 1,
2022
Received in revised form:
June 22,
2022
Received:
February 11,
2022
Identification
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