Aphagia, adipsia, and sensory-motor deficits produced by amygdala lesions: a function of extra-amygdaloid damage.

Small bilateral electrolytic lesions confined to the region of the central nuclei of the amygdala failed to affect food and water consumption in male rats. More medially-placed lesions which damaged portions of the internal capsule, entopeduncular nucleus and globus pallidus adjacent to the central nucleus produced transient aphagia and adipsia accompanied by sensory-motor impairments that interfered with the act of feeding, as evidenced by a large postoperative increase in the amount of food spilled. In some cases lesions restricted to the internal capsule and entopeduncular nucleus produced these sensory-motor deficits but no aphagia or adipsia. Small lesions damaging primarily ventral portions of the posteromedial pallidi resulted in aphagia and adipsia but no apparent sensory-motor impairment. The results indicate that at least two, possibly independent, deficits in food intake may be produced by lesions in the immediate area of the dorsomedial amygdala. It is suggested that the effects on ingestive behavior which several investigators have observed in rats with dorsomedial amygdaloid damage may in fact be due to incidental destruction of adjacent tissues.