Morphine induces antinociception by activating μ opioid receptors (μORs) in spinal and
supraspinal regions of the CNS. βarrestin-2 (βarr2), a G-protein-coupled receptor-regulating …

G protein-coupled receptor regulation by G protein-coupled receptor kinases and β-arrestins
can lead to desensitization and subsequent internalization of the receptor. In in vitro and …

Ligands acting at the same receptor can differentially activate distinct signal transduction
pathways, which in turn, can have diverse functional consequences. Further, receptors …

Chronic morphine treatment produces behavioral and cellular opioid tolerance that has
been proposed to be caused by attenuated μ-opioid receptor (MOR) recovery from …

Morphine is a potent analgesic, yet, like most opioid narcotics, it exerts unwanted side
effects such as constipation and respiratory suppression, thereby limiting its clinical utility …

The reinforcing and psychomotor effects of morphine involve opiate stimulation of the
dopaminergic system via activation of μ-opioid receptors (μOR). Both μ-opioid and …

Chronic opioid receptor (OR) activation by morphine causes distinct cellular adaptations
responsible for the development of tolerance. The present study examines the effect of …

Morphine is a widely used analgesic in humans that is associated with multiple untoward
effects, such as addiction and physical dependence. In rodent models, morphine also …

Agonists acting on µ‐opioid receptors (MOR) are very effective analgesics but cause
tolerance during long‐term or repeated exposure. Intensive efforts have been made to find …

It has been demonstrated that opioid agonists that preferentially act at μ-opioid receptors to
activate G protein signaling over βarrestin2 recruitment produce antinociception with less …