As social creatures, we are impacted by the mere presence of our conspecifics. Behavioural adaptations, such as an increased drive for social interaction following isolation, have been linked to circuit changes involving oxytocin signalling, but the underlying molecular and cellular changes remain unclear. We used a juvenile social isolation paradigm, wherein male mice are single-housed between P21-P28, and their social behaviour is subsequently examined in a five-trial social recognition / interaction test. In this assay, we observed a lack of social habituation, whereas social recognition was intact. We hypothesise that this behavioural adaptation is connected to plasticity of oxytocinergic neurons in the paraventricular nucleus of the hypothalamus (PVN), where oxytocin is primarily synthesised. We are now examining plasticity at the level of oxytocin expression and the synaptic inputs formed onto the PVN oxytocin cells. In our experiments, we employ recombinant fibronectin intrabodies (FingRs) – a tool that allows us to individually label excitatory or inhibitory synapse formed onto genetically-defined neuron populations. In future steps, we want to also address social isolation-induced plasticity at the level of PVN output connectivity.