The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract.
J Mol Med. 2005-08-26; 83(12): 944-954
DOI: 10.1007/s00109-005-0698-5
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1. J Mol Med (Berl). 2005 Dec;83(12):944-54. Epub 2005 Aug 26.
The endocannabinoid system in the physiology and pathophysiology of the
gastrointestinal tract.
Massa F(1), Storr M, Lutz B.
Author information:
(1)Department of Physiological Chemistry, Johannes Gutenberg-University Mainz,
Duesbergweg 6, 55099 Mainz, Germany.
Numerous investigations have recently demonstrated the important roles of the
endocannabinoid system in the gastrointestinal (GI) tract under physiological and
pathophysiological conditions. In the GI tract, cannabinoid type 1 (CB1)
receptors are present in neurons of the enteric nervous system and in sensory
terminals of vagal and spinal neurons, while cannabinoid type 2 receptors are
located in immune cells. Activation of CB1 receptors was shown to modulate
several functions in the GI tract, including gastric secretion, gastric emptying
and intestinal motility. Under pathophysiological conditions induced
experimentally in rodents, the endocannabinoid system conveys protection to the
GI tract (e.g. from inflammation and abnormally high gastric and enteric
secretions). Such protective activities are largely in agreement with anecdotal
reports from folk medicine on the use of Cannabis sativa extracts by subjects
suffering from various GI disorders. Thus, the endocannabinoid system may serve
as a potentially promising therapeutic target against different GI disorders,
including frankly inflammatory bowel diseases (e.g. Crohn’s disease), functional
bowel diseases (e.g. irritable bowel syndrome) and secretion- and
motility-related disorders. As stimulation of this modulatory system by CB1
receptor agonists can lead to unwanted psychotropic side effects, an alternative
and promising avenue for therapeutic applications resides in the treatment with
CB1 receptor agonists that are unable to cross the blood-brain barrier, or with
compounds that inhibit the degradation of endogenous ligands (endocannabinoids)
of CB1 receptors, hence prolonging the activity of the endocannabinoid system.
DOI: 10.1007/s00109-005-0698-5
PMID: 16133420 [Indexed for MEDLINE]