We compared the magnitude of devaluation deficits in the present study to those in our prior reports following microinjection of MUS into either the BLA or OFC (Wellman et al., 2005; West et al., 2011). The only other primate study to employ inactivation methods in the reinforcer devaluation task used a different agent (THIP) (Murray et al., 2015) so we were unable to compare those data to experiments conducted using MUS. Moreover, all prior studies of the thalamus in the reinforcer devaluation task have used permanent lesions, rather than inactivation (Izquierdo et al., 2004; Izquierdo and Murray, 2010; Browning et al., 2015), and thus were not compared to the present study. Note that West and colleagues (2011) did not attempt to dissociate between the effects of inactivation of Area 11 and Area 13. Further, note that the Wellman study (2005) only found a deficit after injection before satiation, and not when MUS was injected prior to the probe. Thus, only data from the infusion before satiation condition are included. To compare across these studies, we normalized the proportion shifted after drug infusion to the proportion shifted after control infusions. Normalization was required, as the raw proportion shifted under saline conditions differed substantially across these studies. Proportion shifted values for drug-infused sessions were expressed as a percent of the value during the control session, thus, a value of 100% indicates no deficit. In all cases, a one-tailed, one sample T-test (against a test value of 100, i.e. no change from control) confirmed the presence of deficits compared to control conditions. [Wellman et al., Before Satiation: t = 3.8, df = 5, p=0.006; West et al., Before Satiation: t = 2.47, df = 3, p=0.045; Present Study, Before Satiation: t = 5.73, df = 3, p=0.005; West et al., Before Probe: t = 2.68, df = 3, p=0.0375; Present Study, Before Probe: t = 4.38, df = 3, p=0.011]. We next analyzed the normalized proportion shifted for the three studies when MUS was infused before satiation. Analysis of Variance did not reveal a significant treatment effect (F2,11=2.768, p=0.106), but consistent with visual observation of the data, there was a non-significant trend towards a difference between the effect in the present study and that reported in Wellman et al., p=0.084, Dunnett's test). We next compared the proportion shifted when MUS was infused prior to the probe test in West, et al., to that in the present study. Unpaired t-test showed that the magnitude of devaluation did not differ between these conditions (t=0.4691, df=6, p=0.6555). These data suggest that deficits caused by inactivation of any of these regions are similar in magnitude, although, in the case of infusion before satiation, there is a trend toward more severe deficits after inactivation of BLA. The symbols used for the present study follow the conventions in the other figures. Diamonds show individual animals for the other studies. In all cases, the deficits we observed fell within the range of deficits previously reported after inactivation of the BLA and OFC.