Impairments in saline intake induced by deposit-free electrolytic lesions in the thalamic gustatory area.

Previous studies demonstrating impairments in sodium appetite following destruction of the thalamic gustatory relay of the rat utilized lesion procedures which depositd irritative ferric ions around the lesion site. The present study used a deposit free lesioning procedure to determine whether the disruption in sodium appetite is attributable to factors other than tissue destruction. The results showed that deposite free lesions produce deficits in sodium appetite which are similar in specificity, intensity, and uniformity to those produced by irritative lesion procedures.