====== Mu opioid receptor ======


Its a major subtype of [[opioid receptor]]

mu (μ)
MOR
OP3 (I)	μ1, μ2, μ3	
brain
cortex (laminae III and IV)
thalamus
striosomes
periaqueductal gray
rostral ventromedial medulla
spinal cord
substantia gelatinosa
peripheral sensory neurons
intestinal tract
μ1:
analgesia
physical dependence
μ2:

respiratory depression
miosis
euphoria
reduced GI motility
physical dependence
μ3:

possible vasodilation
----
The aim of a [[study]] of Ji and Wang from the [[Cangzhou Central Hospital]], was to investigate the role of μ-[[opioid receptor]]s in [[acute respiratory distress syndrome]] and whether their protective effect is mediated via [[PI3K/AKT/mTOR pathway]]. What is the main finding and its importance? The findings show that activation of μ-opioid receptors ameliorates [[lung injury]], effects reversed by the PI3K inhibitor, [[wortmannin]].

The main pathology of acute respiratory distress syndrome (ARDS) is the accumulation of inflammatory cells in the [[lung]] and increased permeability of vascular [[endothelial cell]]s. The μ-opioid receptor (MOR) is a [[G protein coupled receptor]], which stimulates [[angiogenesis]] and vascular endothelial cell proliferation. In addition, MOR inhibited [[cell]] [[apoptosis]] via PI3K/Akt signaling pathway. In this study, they aimed to explore the contribution of MOR in ARDS and whether effects are mediated via PI3K/Akt signalling. An ARDS model was established by intra-tracheal instillation of 5 mg k-1 g [[lipopolysaccharide]] (LPS). Lung injury was confirmed by [[hematoxylin]] and eosin staining, lung wet/dry weight ratio, bronchoalveolar lavage fluid (BALF) protein concentrations, [[myeloperoxidase]] (MPO) activity and vascular cell adhesion molecule 1 (VCAM-1) expression. Lung inflammation was determined by assessment of [[interleukin]]-1beta (IL-1β) and tumor necrosis factor alpha (TNF-α) concentrations. The protein levels of p-Akt was detected by [[western blot]]. Endomorphin-1-activated MORs attenuated LPS-induced lung injury, lung wet/dry weight ratio, BALF protein concentrations, MPO activity, IL-1β and TNF-α levels and VCAM-1 expression, and elevated LPS-induced decreased p-Akt expression. However, the protective effect of MOR activation on lung injury was reversed by the PI3K inhibitor, wortmannin. In conclusion, μ-opioid receptor involvement in LPS-induced ARDS is via the PI3K/Akt pathway
((Ji S, Wang L. The role of μ-opioid receptors in respiratory distress syndrome 
μ-opioid receptor signalling via PI3K/Akt pathway ameliorates
lipopolysaccharide-induced acute respiratory distress syndrome. Exp Physiol. 2019
Jul 4. doi: 10.1113/EP087783. [Epub ahead of print] PubMed PMID: 31272134.
)).