There is also some preliminary evidence for an interaction between the oxytocinergic and noradrenergic system. In support of this mechanism, pretreatment with OXT attenuated reinstatement of alcohol-seeking in mice (King and Becker, 2019) and methamphetamine-seeking in rats (Cox et al., 2013, Everitt and Robbins, 2013) induced by yohimbine, an alpa-2 receptor antagonist. Further, the ability of OXT to attenuate morphine-primed reinstatement of CPP in mice has been associated with the ability of OXT to suppress striatal noradrenaline turnover (Georgiou et al., 2015). Oxytocin administration has been shown to enhance noradrenaline release in the SON, whereas stressful stimuli and food intake activate hypothalamic OXT neurons, at least in part, by noradrenergic neurons in the nucleus tractus solitarius (Onaka et al., 2012). Oxytocin receptors may also interact with a2 adrenergic receptors (a(2A)ARs) in a similar fashion (Fuxe et al., 2012) to dopamine receptors. More specifically, OXT via signaling at OXTR-a(2A)AR heteroreceptor complex may act as an allosteric antagonist to reduce adrenergic signal transduction (Diaz-Cabiale et al., 2000). It is also likely that a(2A)ARs can also modulate OXTRs through reciprocal receptor-receptor interaction (Fuxe
