This study investigated a causal relationship between anorexia and anhedonia in an animal model of stress, and examined if the stress-induced anorexia and/or anhedonia is accompanied by changes in sweet receptor expression in taste cells. Rats received daily injections of dexamethasone (0.1 or 1 mg/kg) or saline, mimicking stress status. Anhedonia was assessed by measuring preferences for sweet and palatable foods at different time points of drug injections. Rats were subjected to behavioral sessions to assess depression-like behaviors after 3 days or 4 weeks of daily drug injections. Decreased food intake was observed from the first day of dexamethasone injection in a dose dependent manner, and persisted throughout the whole experimental period, revealing anorectic property of the drug treatment. Sucrose preference was decreased in the 2nd week, and cookie consumption on the 4th day, of drug treatment, as the earliest time point, respectively. Increased immobility during forced swimming test was observed at the 3rd week, but not on the 4th day, of drug treatment. Sweet receptors, T1R2 and T1R3, expression in the circumvallate papillae was not affected by dexamethasone treatment. It is concluded that the development of anhedonia, possibly caused by anorexia, is a pre-symptomatic feature of depression in rats treated with chronic dexamethasone, and its pathophysiologic mechanisms may not comprise changes in sweet receptor expression in taste cells.