Two weeks after parasagittal hypothalamic knife cuts, baseline eating was elevated and 300 mg/kg 2 deoxy-D-glucose (2DG) did not further stimulate food intake. Five weeks postoperatively the food intake baseline had fallen and an eating response to 300 mg/kg 2DG was now seen (p less than 0.005). In this delayed (static) phase intake was also stimulated by 150 mg/kg 2DG (p less than 0.005). 600 mg/kg did not stimulate intake in the lesioned rats at any time, although sham-operated rats always responded positively to this high dose. In conclusion, the neural substrate damaged in hypothalamic hyperphagic rats does not appear to mediate eating in response to glucopribation. The eating response is masked by high baseline intake in the dynamic phase, but reappears in the static phase.