It is commonly believed that salt intake is required solely to maintain mineralofluid balance, and that its excessive intake is pathophysiological. Yet, apart from the increased intake of sodium-rich foods caused by perinatal sodium loss, the determinants of human salt intake, its excess and persistence, are unknown. One suggestion is that high salt intake may be adaptive in coping with daily adversity. Therefore, we investigated the effect of low dietary sodium in models of depression and anxiety, on chronic mild stress (CMS), and on acute unpredictable stressors. We find that low dietary sodium exacerbates anxiety in the elevated maze and open field. However, it does not exacerbate modeled depression or anxiety in chronically and acutely stressed rats. We find that CMS-induced anhedonia reduces 1.5% NaCl as well as 5% sucrose intake. The reduction in NaCl intake is specific to depression insofar as it did not occur after repeated acute stressors. The reduction occurred despite sodium restriction. Thus while sodium restriction is anxiogenic, it does not exacerbate preexisting depression or anxiety in clearly demarcated behavioral models. These psychological dimensions of salt intake are only now being addressed experimentally, and the ramifications for its control, and for individuals vulnerable to depression or stress, require clarification.