Persisting gaps in M-OUD coverage at post-discharge recovery houses necessitate our continued advocacy.

Effective treatment of opioid use disorder (OUD) must target both the medical and psychosocial aspects of a patient's condition. This, in turn, requires a collaboration between medical providers and social supports. We would like to illustrate a key difficulty in this collaboration for some patients in our country: many post-discharge recovery houses continue to refuse to allow patients to remain on medication treatment for OUD (M-OUD). This barrier to M-OUD access in recovery houses is a significant obstacle to effective OUD treatment.

Endocannabinoid signalling modulates susceptibility to traumatic stress exposure.

Stress is a ubiquitous risk factor for the exacerbation and development of affective disorders including major depression and posttraumatic stress disorder. Understanding the neurobiological mechanisms conferring resilience to the adverse consequences of stress could have broad implications for the treatment and prevention of mood and anxiety disorders. We utilize laboratory mice and their innate inter-individual differences in stress-susceptibility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resilience. Specifically, systemic 2-AG augmentation is associated with a stress-resilient phenotype and enhances resilience in previously susceptible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previously resilient mice. Moreover, stress-resilience is associated with increased phasic 2-AG-mediated synaptic suppression at ventral hippocampal-amygdala glutamatergic synapses and amygdala-specific 2-AG depletion impairs successful adaptation to repeated stress. These data indicate amygdala 2-AG signalling mechanisms promote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated stress exposure.