Translational regulation plays a key role in synaptic plasticity. However, the critical targets and physiological context of how regulated translation is leveraged for neuronal adaptations is poorly understood. I am testing the hypothesis that social homeostasis engages differential regulation of translation, thereby directing neuronal plasticity for behavioral adaptations. The concept of social homeostasis proposes that social behavior is regulated by a complex feedback system to maintain a stable set-point for social interactions. The oxytocinergic system regulates key elements of social interactions, habituation and reward. There is evidence that the expression of the oxytocin receptor (OXTR), a G-protein coupled receptor (GPCR), is dynamically regulated. We identified three alternative transcription start sites (aTSS) for the mouse Oxtr gene. Interestingly, two of the resulting Oxtr mRNA transcript isoforms contain upstream open reading frames (uORFs) in their 5’ UTRs. Using Luciferase reporter gene assays, we found that these uORFs strongly repress the translational output from the principal open reading frame (pORF) in vitro, raising the possibility that selective translational regulation contributes to social behavior adaptations. To test a regulatory role in vivo, we generated transgenic knock-in (KI) mice with point-mutations in the upstream AUG sequences. Furthermore, we perform ribosome footprinting from socially isolated and group-housed mice, to identify if translation initiation occurs at the uORFs of the Oxtr mRNA and if uORF usage changes upon behavioral adaptations.