Oxytocin has been reported to reduce activity of the HPA-axis under basal conditions as well as following exposure to various stress events/stimuli (Jurek et al., 2015, Neumann et al., 2000b, Peters et al., 2014, Slattery and Neumann, 2010, Knobloch et al., 2012). Oxytocin dampens stress-induced HPA-axis activation (as indexed by elevated circulating corticosteroid levels), as well as reduces stress-related behavioral responses in animal models of anxiety and depression (Neumann et al., 2000a, Windle et al., 2004). More specifically, central OXT administration (icv.) decreased stress-induced corticosterone release in rats (Windle et al., 1997), whereas intra-PVN administration of OXTR antagonist reduced ACTH release in response to force swim stress (Neumann et al., 2000b). Further, at baseline high levels of OXT and OXTR mRNA expression are localized in forebrain regions such as the extended amygdala, where OXT signaling can play a significant role in the regulation of anxiety, stress, and reward-related behaviors (Dabrowska et al., 2011, Gimpl and Fahrenholz, 2001, Veinante and Freund-Mercier, 1997, Martinon and Dabrowska, 2018). Oxytocin was also found to directly attenuate stress-induced synthesis of CRF within PVN via specific
