Ligand-induced μ opioid receptor internalization in enteric neurons following chronic treatment with the opiate fentanyl.

Morphine differs from most opiates its poor ability to internalize μ opioid receptors (μORs). However, chronic treatment with morphine produces adaptational changes at the dynamin level, which enhance the efficiency of acute morphine stimulation to promote μOR internalization in enteric neurons. This study tested the effect of chronic treatment with fentanyl, a μOR-internalizing agonist, on ligand-induced endocytosis and the expression of the intracellular trafficking proteins, dynamin and β-arrestin, in enteric neurons using organotypic cultures of the guinea pig ileum.

Protective role of μ opioid receptor activation in intestinal inflammation induced by mesenteric ischemia/reperfusion in mice.

Intestinal ischemia is a clinical emergency with high morbidity and mortality. We investigated whether activation of μ opioid receptor (μOR) protects from the inflammation induced by intestinal ischemia and reperfusion (I/R) in mice. Ischemia was induced by occlusion of the superior mesenteric artery (45 min), followed by reperfusion (5 hr).

Morphine induces μ opioid receptor endocytosis in guinea pig enteric neurons following prolonged receptor activation.

Background & Aims: The μ opioid receptor (μOR) undergoes rapid endocytosis after acute stimulation with opioids and most opiates, but not with morphine. We investigated whether prolonged activation of μOR affects morphine's ability to induce receptor endocytosis in enteric neurons.

Methods: We compared the effects of morphine, a poor μOR-internalizing opiate, and (D-Ala2,MePhe4,Gly-ol5) enkephalin (DAMGO), a potent μOR-internalizing agonist, on μOR trafficking in enteric neurons and on the expression of dynamin and β-arrestin immunoreactivity in the ileum of guinea pigs rendered tolerant by chronic administration of morphine.