in this study, but might have been the origin of these residual correlations, These include the amygdala (AMY), supramammillary nucleus (SUM), entorhinal cortex (EC), medial septum (MS), and (VTA) (McKenna and Vertes 2004; Cassel et al. 2013; Dolleman-Van der Weel et al. 1994). A monosynaptic PFC-HC projection (mainly from anterior cingulate to CA3/CA2) has also been reported recently (Rajasethupathy et al. 2015). Second, the origin and neuronal mechanisms of the PFC 2–5 Hz oscillation remains unknown. This rhythm is not necessarily generated within the PFC but may be induced by input from VTA (Fujisawa and Buzsaki 2011), from the nRE (Kiss et al. 2011a; Kiss et al. 2011d; Zhang et al. 2012; Duan et al. 2015; Nagy et al. 2016), or through a PFC-nRE reciprocal circuit (Fig. 7B). Our recordings and analysis cannot differentiate between these models; partial correlation finds unique variance between two variables which is not shared by the third variable but does not provide information on where that variance comes from. A model of a thalamo-cortical network depicted in Fig 7B could explain another interesting observation in regard of theta input i.e. controlling for PFC suppressed nRE-HC theta correlation (Fig. 5E). Third, we have only found significant
