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Background: Depression and anxiety are significant health burdens that greatly impact the quality of life of refugees and migrants. In this study, we have translated and culturally adapted the Patient Health Questionnaire (PHQ-9) and Generalized Anxiety Disorder Screener (GAD-7) into Kinyarwanda and performed a validation study in a United States (US) primary care setting. Methods: A committee of seven experts including psychiatric and family medicine providers, health researchers, and trained medical interpreters translated and culturally adapted the PHQ-9 and GAD-7, and incorporated feedback from cognitive interviews with bilingual participants. The translated instruments were then tested in a cross-sectional validation study. Analyses include internal consistency, discriminant validity, principal component analyses, and confirmatory factor analyses. Results: Analyses of 119 responses indicated overall good internal consistency with Cronbach's α of 0.85 (PHQ-9) and 0.92 (GAD-7). Both scales showed acceptable factor loadings between 0.44 and 0.90 in the principal component analyses and showed strong correlations with health-related quality of life and depression/anxiety symptoms measured with visual analog scales. Significantly higher scores for PHQ-9 and GAD-7 were shown among participants with known psychiatric conditions. Discussion: PHQ-9 and GAD-7 demonstrated commendable applicability for Kinyarwanda-speaking patients in primary healthcare settings in the US. Our instruments can already be used in primary care settings and thus help to mitigate health disparities. Future research should further validate our tool against gold-standard diagnostics in larger, geographically diverse samples. [ABSTRACT FROM AUTHOR]

The role of Mu opioid receptor (MOR)‐mediated regulation of GABA transmission in opioid reward is well established. Much less is known about MOR‐mediated regulation of glutamate transmission in the brain and how this relates to drug reward. We previously found that MORs inhibit glutamate transmission at synapses that express the Type 2 vesicular glutamate transporter (vGluT2). We created a transgenic mouse that lacks MORs in vGluT2‐expressing neurons (MORflox‐vGluT2cre) to demonstrate that MORs on the vGluT2 neurons themselves mediate this synaptic inhibition. We then explored the role of MORs in vGluT2‐expressing neurons in opioid‐related behaviors. In tests of conditioned place preference, MORflox‐vGluT2cre mice did not acquire place preference for a low dose of the opioid, oxycodone, but displayed conditioned place aversion at a higher dose, whereas control mice displayed preference for both doses. In an oral consumption assessment, these mice consumed less oxycodone and had reduced preference for oxycodone compared with controls. MORflox‐vGluT2cre mice also failed to show oxycodone‐induced locomotor stimulation. These mice displayed baseline withdrawal‐like responses following the development of oxycodone dependence that were not seen in littermate controls. In addition, withdrawal‐like responses in these mice did not increase following treatment with the opioid antagonist, naloxone. However, other MOR‐mediated behaviors were unaffected, including oxycodone‐induced analgesia. These data reveal that MOR‐mediated regulation of glutamate transmission is a critical component of opioid reward. [ABSTRACT FROM AUTHOR]