Systemic administration of serotonin exacerbates abdominal pain and colitis via interaction with the endocannabinoid system.
Molecular basis of abdominal pain in IBD is not fully characterized. Serotonin (5-HT) increases visceral pain severity and contributes to exacerbation of inflammation. Moreover, it is well established that decreased anandamide (AEA) signaling in the gut increases visceral pain severity. The aim of this study was to investigate the interplay between 5-HT and endocannabinoid signaling in colitis. Our study shows a link between 5-HT and endocannabinoid signaling pathways in IBD. Thus, pharmacological blockade of 5-HT signaling or supplementation with endocannabinoids in the gut might be of benefit in severe cases of abdominal pain in IBD.
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Man and the Microbiome: A New Theory of Everything?
The gut microbiome is now considered as an organ contributing to the regulation of host metabolism. Since the finding of the existence of a relationship between the gut microbiome and specific diseases, numerous studies have also deciphered molecular mechanisms explaining how gut bacteria dialogue with host cells and eventually shape metabolism. Both metagenomic and metabolomic analyses have contributed to the discovery of bacterial-derived metabolites acting on host cells.
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THE GUT MICROBIOME INFLUENCES HOST ENDOCRINE FUNCTIONS.
The gut microbiome is now considered as an organ contributing to the regulation of host metabolism. Since the finding of the existence of a relationship between the gut microbiome and specific diseases, numerous studies have also deciphered molecular mechanisms explaining how gut bacteria dialogue with host cells and eventually shape metabolism. Both metagenomic and metabolomic analyses have contributed to the discovery of bacterial-derived metabolites acting on host cells.
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Altered gut microbiota and endocannabinoid system tone in vitamin D deficiency-mediated chronic pain.
Recent evidence points to the gut microbiota as a regulator of brain and behavior, although it remains to be determined if gut bacteria play a role in chronic pain. The endocannabinoid system is implicated in inflammation and chronic pain processing at both the gut and central nervous system (CNS) levels. In the present study, we used low Vitamin D dietary intake in mice and evaluated possible changes in gut microbiota, pain processing and endocannabinoid system signaling.
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Cannabis, Cannabinoids, and the Endocannabinoid System-Is there Therapeutic Potential for Inflammatory Bowel Disease?
Cannabis sativa and its extracts have been used for centuries, both medicinally and recreationally. There is accumulating evidence that exogenous cannabis and related cannabinoids improve symptoms associated with inflammatory bowel disease [IBD], such as pain, loss of appetite, and diarrhoea. In vivo, exocannabinoids have been demonstrated to improve colitis, mainly in chemical models. Exocannabinoids signal through the endocannabinoid system, an increasingly understood network of endogenous lipid ligands and their receptors, together with a number of synthetic and degradative enzymes and the resulting products. Modulating the endocannabinoid system using pharmacological receptor agonists, genetic knockout models, or inhibition of degradative enzymes have largely shown improvements in colitis in vivo.
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Deficient endocannabinoid signaling in the central amygdala contributes to alcohol dependence-related anxiety-like behavior and excessive alcohol intake.
Negative emotional states that are associated with excessive alcohol intake, particularly anxiety-like states, have been linked to opponent processes in the central nucleus of the amygdala (CeA), affecting stress-related transmitters and monoamines. This study extends these observations to include endocannabinoid signaling in alcohol-dependent animals. Rats and mice were exposed to chronic intermittent alcohol with vapor inhalation or liquid diet to induce dependence. In vivo microdialysis was used to estimate interstitial concentrations of endocannabinoids [N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG)] and amino acids (glutamate and GABA) in rat CeA.
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