), the expression of ENK, DOPr, and MOPr is ubiquitous.
The anatomical distribution of MOPr and DOPr is relatively similar to that of ENK projections .
In the same study, administration of MOPr antagonist (naltrexone) or DOPr antagonist (naltrindole) increased fear response in SWR/J mice, which could be restored with a DOPr agonist.
Positron emission tomography (PET) studies have shown that MOPr expression is decreased in the anterior cingulate cortex of patients with PTSD .
In the same way, the gene inactivation of MOPr has anxiolytic effects, with MOPr KO mice presenting an increased time spent in the open arms of an EPM .
Taken together, the combined findings from these silencing, pharmacological, genetic, and neuroanatomical studies suggest that the stimulation of ENK transmission onto DOPr and/or MOPr might enhance the natural strategies to cope with stress.
Enkephalin Signaling through DOPr and MOPr, a Major Component of the Stress Resilience Circuitry
used the repeated social defeat paradigm in a mouse model of OPRM1 A118G polymorphism (single nucleotide polymorphism, SNP) corresponding to a genetic mutation of MOPr observed in humans that is associated with an overall reduction of baseline MOPr availability in regions implicated in pain and affective regulation , thus allowing to unravel a potential role of MOPr in the resilience to chronic stress .
When considering only one neuropeptidergic system, the ENK acting through DOPr and MOPr, numerous implicated brain structures and circuits emerge (see Figure 1 for a schematic representation that we overlapped with the cartography of main connectivities known to be involved in stress response, fear, and resilience).