“…Consistent with the possibility that one or more of the sites discussed perform this integration, sodium appetite is substantially reduced after lesions in the PB (Flynn et al,1991; Scalera et al,1995), BST (Reilly et al,1994; Zardetto‐Smith et al,1994), CeA (Cox et al,1978; Schulkin et al,1989; Galaverna et al,1992; Zardetto‐Smith et al,1994; Johnson et al,1999), and LHA (Wolf,1964a). Critical contributions from any of the aforementioned subcortical sites, driven by input from the HSD2 neurons, would also be consistent with prior evidence that the brain circuitry underlying sodium appetite requires intact connections between the brainstem and forebrain (Grill et al,1986), but not the gustatory thalamus (Scalera et al,1997) or sensory cortex (Wolf et al,1970; Wirsig and Grill,1982).…”