A large body of evidence exists to support “cross-talk” among the related peptides OXT and vasopressin (AVP) and their receptors, though the mechanisms and functional significance of such OXT-AVP interactions remain poorly understood (Chini et al., 2017; see review: Carter et al., 2017). The two hypophyseal neuropeptide systems generally produce opposing physiological actions; central oxytocin dampens HPA-axis activity and exerts anxiolytic effects whereas AVP enhances CRF-activation of the HPA-axis, increasing anxiety and depressive-related behaviors (Neumann and Landgraf, 2012). Due to high structural homology, OXT also binds to and activates AVP receptor subtypes (V1a, V1b and V2) (Knobloch and Grinevich, 2014). Under some conditions, this may constitute alternative targets for OXT, especially at high local concentrations and in brain regions that have little or no OXTR expression (Grinevich et al., 2016, Manning et al., 2008). Further, adding to the complexity of OXT and AVP interactions is the possibility that OXT and AVP receptors can form heterodimers with unknown results on peptide binding (Chini et al., 2017). Interestingly, a role for AVP has been implicated in the transition to alcohol dependence (Zhou
