The role of endocannabinoids in visceral hyposensitivity induced by rapid eye movement sleep deprivation in rats: Regional differences

Abstract

Abstract. Visceral hypersensitivity is one of the most important mechanisms of functional gastrointestinal diseases. Our previous studies have shown that rapid eye movement (REM) sleep deprivation (REMSD) decreases visceral sensitivity in rats, but the mechanisms involved in this effect, have not yet been clarified. In this study, we investigated the role of the CNS and peripheral endocannabinoids in visceral hyposensitivity induced by REMSD. Animals were randomly divided into the cage-yoked (YC), the REMSD group, which suffered from REMSD for 48 h, and the group with the interventions of Rimonabant after REMSD. The visceral sensitivity of all the groups was assessed, and the expressions of cannabinoid receptor (CB1R), fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MGL) in the CNS and gut regions, were detected. We demonstrate that REMSD decreases visceral sensitivity in rats and that the Rimonabant intervention antagonizes this effect. The expression of CB1R in the CNS region was significantly higher in the REMSD compared to the YC group. We did not see similar results in the gut. At the same time, the expressions of FAAH and MGL in the CNS and colon, excluding the iliac terminus, were lower in the REMSD compared to the YC group. Endocannabinoids are involved in the mechanism of visceral hyposensitivity in rats induced by REMSD. Possibly those in the CNS play the main role in this activity.

Endocannabinoid Signaling in the Etiology and Treatment of Major Depressive Illness

“…Although insomnia is highly prevalent in patients with depression and is an important diagnostic criterion and risk factor for depression [266], sleep deprivation (wake therapy) provides rapid clinical relief in many patients [267, 268]. Deprivation specifically from rapid eye movement (REM) sleep increases the expression of CB1R in the thalamus, brain stem and spinal cord and decreases expression of both FAAH and the 2-AG catabolic enzyme, MGL [269]. Sleep deprivation increases 2-AG concentrations in the hippocampus [270] and increases circulating eCBs in humans [271].…”